Warning new off gassing product!!!!

[u.g.u]

more pics

u.g.u Reviewed by u.g.u on 09-17-2010. Warning new off gassing product!!!! So I have been experiencing a mysterious yellowing for about 10 months. Every thing that went into one of my 11 different rooms (some that had been going 5+ years) started to yellow and eventually die. My first instinct was my ph I checked my pens, they were not very far off but I calibrated and bought new probes anyways. That did nothing. Then we suspected the nutes, maybe we got a bad batch. I had bought 6 gallon jugs and filled all my 1 galâ??s up off the same batch. Call the company run Rating: 5

[u.g.u]

How do I identify phthalates in products?
There is no easy way to tell if a product has added phthalates. Phthalates can be identified on labels by a three or four letter acronym that defines their chemical structures. Labels rarely state â??contains phthalatesâ?�.
There are a multitude of phthalate compounds. Which phthalate compound is added to a product depends in part on their molecular weight (MW). Phthalates with a higher molecular weight (HMW) are very slightly soluble in water; phthalates with a lower molecular weight (LMW) are reasonably soluble in water.
The 8 most widely used phthalate compounds and their metabolites are:
â?¢ BBP: butyl benzyl phthalate (LMW) *, **, ***
MBzP: mono benzyl phthalate
â?¢ DBP: di-n-butyl phthalate (LMW) *, **, ***
MBP: mono-n-butyl phthalate
MiBP: mono-isobutyl phthalate
Most common phthalate added to nail polish.
â?¢ DEHP: di-(2-ethylhexyl) phthalate (HMW) *, **, ***
MEHP: mono-(2-ethylhexyl) phthalate
Most widely-added phthalate to polyvinyl
chloride (PVC) to make products flexible.
â?¢ DEP: diethyl phthalate (LMW)
MEP: monoethyl phthalate
Most common phthalate added to personal
care products to enhance fragrance.
â?¢ DiDP: di-isodecyl phthalate (HMW) *, **, ***
â?¢ DiNP: di-isononyll phthalate (HMW) *, **, ***
Most common phthalate added as a softener
in the manufacture of toys and childcare products, such as bath toys, drinking straws,
and rubber ducks.
â?¢ DnHP: di-n- hexyl phthalate *
â?¢ DnOP: di-n-octyl phthalate (LMW) **, ***
* Listed in Californiaâ??s Proposition 65 as a reproductive and developmental toxicant.
** Listed in Californiaâ??s AB1108 (Ma and Huffman). The bill, if passed, will ban use in the manufacture of any toy or childcare article intended for use by a child under three years of age.
*** European Union banned as a phthalate softener in the manufacture of toys and childcare articles.
Read Labels to avoid phthalates.
The most common products using phthalate compounds are:
PVC Products
Phthalates are frequently added to PVC (vinyl) products to soften and make more flexible. If a plastic product is flexible, it probably contains phthalates unless the label specifically says it does not.
Personal Care Products
Phthalates are often added to personal care products, such as nail polish, perfumes, deodorants, hair gels, shampoos, soaps, hair sprays, and body lotions, to help lubricate other substances in the formula and to carry fragrances. Phthalates must be listed among the ingredients on product labels, unless they are added as a part of the â??fragrance.â?� Under current law, they can then simply be labeled â??fragrance,â?� even though they may make up 20% or more of the product.
Many companies have voluntarily removed phthalates from their products. A company will usually label its product â??phthalate-free.â?� If unsure, call the company. If you canâ??t get information from the manufacturer, look for alternatives.
How can I recognize plastic toys and
containers containing phthalates?
All plastics are not the same. One easy way to recognize plastic toys, clothing, bottles, food and beverage storage containers, and/or food wrap that may contain phthalate compounds is to look for the number 3 inside the universal recycling symbol usually molded into the plastic on the bottom of the product.
Avoid products with the number 3 within the arrows and the letters â??Vâ?� or â??PVCâ?� below the arrows.
Choose products with the numbers 1,2, 4 and 5 within the arrows. Many companies use phthalate-free substances such as polypropylene (PP), recycling code 5, to manufacture plastic products

[Ocotillo]

scrumby
Well for 1 the problem is not that it is getting into the medium it is offgassing off the tube into the air were it is taken in by the stoma. Then once inside it disrupts the chlorophyll prodution. And 2nd DBP and DIBP are the most unstable and most prone to offgas than any other phthalate. Not to mention the EU has banned the 2 chemicals in all horticultural supplies because of this same reason. So do a little research here I helped you out read the following paragraphs.

Journal of Experimental Botany, Vol. 37, No. 179, pp. 883S97, June 1986
Phytotoxicity of Phthalate Plasticisers
1. DIAGNOSIS AND COMMERCIAL IMPLICATIONS
J. W. HANNAY1 AND D. J. MILLAR2
Department of Pure and Applied Biology, Imperial College, Prince Consort Road,
London SW7 2BB, U.K.
Received 16 October 1985
ABSTRACT
Hannay, J. W. and Millar, D. J. 1986. Phytotoxicity of phthalate plasticisers. 1. Diagnosis and
commercial implicationsâ??J. exp. Bot. 37: 883-897.
The toxicity caused by a volatile constituent from certain samples of flexible polyvinyl chloride (PVC)
was due to dibutyl or diisobutyl phthalate (DBP or DIBP) plasticisers. It has caused serious financial
losses in the horticultural industry. The two phthalate esters have low volatilities, so any toxicity lasts
for many years. Radish (Raphanus sativus L. cv. Cherry Belle) seedlings, exposed to an air stream
containing 160-180 ng dm~3 of butyl phthalates developed chlorotic leaves within 3-4 d and died
within 12 d. Neither dioctyl nor diisodecyl phthalate (DOP nor DIDP) produced damage in the test
plants. Measurements of photosynthetic and respiratory gas exchange in intact shoots of affected
radishes showed that photosynthesis was severely inhibited whilst respiration was virtually
unaffected. Electron micrographs of sections from young leaves showed disruption of thylakoid
formation and granal stacking. In mature leaves, thylakoids and grana were well formed but
chloroplasts were swollen and the thylakoids were pushed towards the vacuolar side of the
chloroplast. Sensitivity to toxic phthalates varies between species; all members of the Crucifcrae tested
were susceptible, tomato less so, and lettuce and ryegrass were resistant. Toxicity of DIBP, from PVC
glazing strip, caused a reduction in crop value of £20000 per acre per year in commercially grown,
monocrop tomatoes.
Key wordsâ??Phthalates, plasticised PVC, radish bioassay, glasshouse, tomato, toxicity.
Correspondence to: Brunei Institute for Bioengineenng, Brunei University, Uxbridge, Middlesex
UP8 3PH, U.K.
INTRODUCTION
A tomato crop failure during the winter of 1978-79 was traced to the introduction of some
flexible polyvinyl chloride (PVC), used in a novel plant supporting system. This PVC gave off
a volatile component which was toxic to tomato but even more toxic to radish. A note was
published in the Grower (Hannay, 1980) warning nurserymen of the potential hazard from
flexible PVC especially in enclosed spaces such as glasshouses during wintertime. On seeing
this publication, a correspondent drew attention to an advertising leaflet issued by BASF,
probably around 1976 ('Plasticised PVC in Horticulture'). The leaflet describes experiments
in which several crop plants were grown in each of four temporary greenhouses; three
covered with PVC film each plasticised with a different phthalate to be compared with one
covered with polythene film as a control. The greenhouse containing DBP as a plasticiser was
toxic to several crop species, whereas those greenhouses having PVC plasticised with either
1 Present address: 18 Goddington Chase, Orpington, Kent BR6 9EA, U.K.
2 Present address and to whom correspondence should be sent: Brunei Institute for Bioengineering, Brunei
University, Uxbridge, Middlesex UP8 3PH, U.K.
© Oxford University Press 1986
Downloaded from Oxford Journals | Life Sciences | Journal of Experimental Botany by Brandon Eckel on July 9, 2010
884 Hannay and Millarâ??Phytotoxicity of Phthalate Plasticisers
diethylhexyl phthalate (DEHP) or diisodecyl phthalate (DIDP) were not toxic. Apparently
the experimental work was carried out in 1970-71 in response to litigation over some flexible
PVC sheet which had proved to be similarly toxic in commercial use: no other details of this
work have been published (private communication). Subsequent enquiries revealed several
papers in Japanese dating from the early 1970's of which the comprehensive paper by Inden
and Tachibana (1975) is the only one which has been translated.
Before embarking on the experimental work it may be helpful to give a brief explanation
of the nature of plasticisers. A plasticiser is used to impart flexibility to a compound and it is
common to have 30-40% by weight of plasticiser in the flexible PVC used in tubing and
sheeting. Several kinds of plasticiser can be used but the most common are the dialkyl
phthalates. Industrially these are made from phthalic anhydride and an alkyl alcohol in the
presence of p-toluene sulphonic acid:
-COOR
-COOR
R may be straight chain or branched. The common R groups are:
(a) Butyl or isobutylâ??to give DBP or diisobutyl phthalate (DIBP).
(b) Ethylhexylâ??to give DEHP, often referred to in the literature as dioctyl phthalate
(DOP) since the straight chain n-octyl is hardly used. DEHP is the most commonly
used phthalate plasticiser accounting for around 25% of world production of
phthalates.
(c) Isooctylâ??diisooctyl phthalate (DIOP) a mixture of octyl alcohols.
(d) Isodecylâ??DIDPâ??together with DIOP this accounts for a further 25% of production.
(Sears and Darby, 1982.)
DBP and DIBP have excellent plasticising properties but have lost favour with the plastics
industry because of their higher volatility compared to phthalates of higher molecular
weight. Their toxicity to plants is a new factor but their effects on animals have been a
concern since the early 1970's (Autian, 1973).
MATERIALS AND METHODS
Plastics
Plastics were prepared in standard, clear rod format to specified formulations (as detailed in the text) by
ICI Plastics and Petrochemicals Division. Commercial glasshouse glazing strip was removed from
glasshouses under the auspices of officers of the Agricultural Development and Advisory Service
(ADAS) and was forwarded to us with appropriate documentation by the officer. The Technical
Services Department at ICI carried out the chemical analyses of the plastics.
Plants
Radish seedsâ??Raphanus sativus L. cv. Cherry Belleâ??were sown in a mixture of equal parts of
Levington Potting Compost and John Innes No. 2 Compost. After 7 d they were transplanted into
small seedtrays (220 mm x 165 mm x 50 mm) so that each tray contained nine plants in rows of three.
The plants were grown in a greenhouse at approximately 23 °C under natural lighting: in winter this
was supplemented with 400 W mercury fluorescent lamps. Prior to use in the bioassay young plants
were transferred for 1 d to the controlled environment room at 22 ± 1 °C and with a photon fluence
rate 185 /imol m'2 s"1 {PAR) from nine, 8 ft 125 W warm white fluorescent tubes plus four 60 W
tungsten lamps for a photoperiod of 18 h d~'.

886 Hannay and Millarâ??Phytotoxicity of Phthalate Plasticisers
Light measurements
Light measurements were made with a Li-Cor Quantum Meter Model LI 185.
Gas liquid chromatography
A Pye Series 104 Model 4 gas chromatograph was used with a flame ionisation detector. The glass
column (500 mm x 2 mm i.d.) was packed with 3% Dexsil 300 on 80-100 mesh Chromosorb G, and the
oven temperature was normally 230 °C. The carrier gas was oxygen-free nitrogen at 40 cm3 min"1;
hydrogen flow rate was also 40 cm3 min"1.
Glass sampling tubes (90 mm x 4 mm i.d.) were thoroughly cleaned with Spectrograde cyclohexane
(Fisons) and then heated to 300 °C for 4 h. One end of each tube was clearly marked with a diamond
marker. Tenax GC 60-80 mesh (Phase Sep) was used to pack the cleaned tubes. The Tenax had also
been preconditioned by heating to 300°C in a stream (40 cm3 min" ') of oxygen-free nitrogen for 24 h.
The filled tubes were closed at each end with caps fashioned from polythene tubing, when not in use.
Immediately prior to use they were purged with nitrogen at 100 cm3 min""1 at 300°C for 10 min.
Sampling of growth chamber atmosphere
Volatile phthalate esters were collected by drawing a known volume of air from the growth chamber
through the glass sample tube packed with Tenax. Normally the sampling was for a period of 48 h. The
flow rate was regulated to 180-200 cm3 min"1 and the total volume of air passing through the Tenax
tube was measured with a dry-type gas meter. Phthalate collected by the Tenax was desorbed by adding
0-5 cm3 cyclohexane into the unmarked end of the tube and allowing it to percolate through. The eluate
was collected in a graduated micro-vial; when the first 0-5 cm3 had percolated through, a second and
then a third 0-5 cm3 was added. The total volume of eluate collected was 1-0 cm3 and the vial was
immediately stoppered. Aliquots (50 mm3) were used for injection into the gas chromatograph.
Calibration curves were prepared by making known additions of individual phthalates into Tenax
tubes and eluting as outlined above.
Care was taken to minimize contamination from extraneous phthalates which are common
pollutants in the environment (Crosby and Singmaster, 1973; Giam, Chan, and Neff, 1975a, b; Gross
and Colony, 1973). All glassware was washed in Spectrograde cyclohexane and heated to 230 °C for
several hours immediately prior to use; polythene end caps were stored at 60 °C until used.
Infrared gas analysis
CO2 exchange was measured using an Infrared Gas Analyser (IRGA) type GC 225.2A (Analytical
Development Company Ltd., England). The IRGA was connected to the test chambers through a
three-way valveâ??Fig. 2(a). Air from a standard air cylinder (British Oxygen Co.) flowed through each
of the three chambers at 200 cm3 min"1. Only the shoots of the plants were exposed inside the plastic
bag; the roots and pot were excluded by placing a perspex base around the hypocotyl and sealing with
lanolinâ??Fig. 2(b). The volume enclosed in the chamber was about 600 cm3. The three plants were
illuminated by four, 5 ft 80 W warm white fluorescent tubes plus two 25 W tungsten bulbsâ??which gave
a photon fluence rate 135 /jmol m~2 s"1 (PAR) at the mid-height of the chambers.
Using a multi-channel switching unit, air could be passed through a valve to the IRGA, or exhausted
to the outside. Air from each chamber flowed through the IRGA for 10 min before switching to the next
chamber.
Electron microscopy
Small pieces of leaf (approximately 2-3 mm2) were excised from a region halfway along the lamina
between the midrib and the leaf margin of treated and untreated leaves. These were placed immediately
in a solution of 2-5% glutaraldehyde (EM grade, EM-scope) fixative in a 100 mol m " 3 cacodylate buffer.
Each excised piece of leaf was then cut into smaller pieces under the glutaraldehyde (approximately 0-25
mm2 in area). The samples were then fixed for 24 h at room temperature, post fixed in osmium tetroxide
and then routinely processed (Glauert, 1980). Cut sections were 60 nm thick and were stained in uranyl
acetate and lead citrate.
RESULTS
Certain plastics are toxic
Using the bioassay system illustrated in Fig. 1 it was possible to identify those combinations
of PVC resin, plasticiser and stabiliser which were toxic and thus to identify the constituent

TABLE 1. Formulations of plastics supplied by ICI
Numbers are parts by weight of each constituent.
Formulation
PVC
DBP
DEHP
ESBO"
Stearic acid
Ba/Cd stabiliser
Ca/Zn stabiliser
Chlorosis and death
in bioassay
Plastic
A
100
42
^_
â??
m2â??
+
B
100
42
0-2
2
â??
_
C
100
42
0-2
2
â??
D
100
42
â??
â??
2-5
+
E
100
.. ..
42
,â??,
â?¢ _
â??
2-5
F
100
..
.
42â??
â??.
2-5
" Epoxydised soya bean oil.
which caused toxicity. The various formulations were made up into approximately 70 mm
diameter clear rod by ICI.
The plastic rod was cut into 10 cm lengths for ease of packing and to ensure a fairly
turbulent flow over the surfaces. The glass tubes were packed with 170 g of plastic for
bioassay. The same sample could be used repeatedly, since the toxin continues to volatilize at
room temperature for several years.
Formulations A and D caused obvious chlorosis within a few days and the plants were
dead within about 12 d. Formulations B, C, E and F caused no obvious differences from the
controls. The only thing in common between samples A and D were the PVC resin and the
plasticiserâ??which was DBP.

FIG. 3. The effect of continuing exposure to the vapour from various samples of PVC on increase in
weight of radish seedlings. (Each point is the mean of three individual weights.)
Chemical analysis of, the original clear plastic tubing which had started these investigations
had showed that it contained DBP as plasticiser. The black plastic from the
Humberside tomato nursery had a mixture of diisobutyl phthalate (DIBP) and diisooctyl
phthalate (DIOP) as its-plasticiser. DIBP might account for it's toxicity, whereas DIOP has
not been shown to be toxic. A further batch of plastics were prepared by ICI, on a similar
basis to those already used, containing DIBP, DIOP, DNP and DIDP. Only DIBP was
toxic. In fact no plastic so far tested in our bioassay has been found to be toxic unless it
contained either DBP or DIBP.
When the plastics were prepared by ICI a sample of each constituent was taken from the
identical batch so that each could be tested separately. Preliminary tests with the pure
plasticiser did not confirm the toxicity of the butyl phthalates. Then it was realised that the
surface area of the liquid plasticiser being presented was considerably less than the surface
area of the pieces of plastic rod normally used. When a filter paper 'sail' was erected in the
long, narrow, glass 'boat' in which the plasticiser was contained, so that the total surface area
was equal to that of the plastic, then chlorosis occurred quite quickly and the radishes died
within about 14 d. If the surface area of the plasticiser was reduced to about one third that of
the plastic then the toxicity was much less than from the plastic. This suggests that the
plasticiser must form a film on the surface of the plastic, since it only constitutes about one
third of the total mass.
With equal weights and similar surface areas of three plastics the results shown in Fig. 3
were obtained.
Only the plastic containing DBP produced an obvious difference in weight from the
control. The DBP-treated plants after 10 d had produced three leaves whereas the controls
had four. Moreover, the leaves of the DBP-treated plants were by now withered and some

cotyledons had also started to collapse. Cotyledons which were still turgid remained green.
In contrast to this the leaves of the control plants were healthy and greenâ??as were their
cotyledons. Chlorosis was beginning to show in DBP-treated plants after 3 d together with
curling of some leaves. At 6 d chlorosis was developing in the veinal regions of older leaves.
The youngest leaf on these plants did not develop any chlorophyll. This is typical of the effects
of both DBP and DIBP, either when incorporated into flexible PVC or as pure substances.
Glazing strip in some glasshouses causes toxicity
In February 1983, we first became aware of a disorder which was afflicting tomato plants in
a few commercial glasshouses. It's cause was unknown but Mr N. Starkey, the officer in
charge of tomato cultivation trials at the Efford Experimental Station of ADAS was
convinced that the toxin was in the atmosphere but had eliminated most of the obvious
possibilities such as ethylene, propylene and sulphur dioxide. After further investigation he
concluded that the most likely source of toxin was the PVC glazing strip. This is the 'cushion'
of thin PVC tubing on which the sheets of glass are bedded to separate them from the
aluminium frame and to give an air-tight seal.
A sample of this glazing strip was tested in our bioassay and was found to be very toxic. A
similar sample from a commercial tomato nursery in which similar toxicity symptoms were
appearing, was also toxic. However, glazing strip from an adjacent glasshouse, on the same
site and planted with the same cultivar, was found to be non-toxic in the bioassay. This was
anticipated since it was not causing any disorder in the glasshouse tomatoes. Chemical
analysis of the two toxic glazing strips revealed that both contained approximately equal
amounts of DIBP and DEHP whereas the non-toxic strip contained only DEHP. The
non-toxic strip came from an older glasshouse whereas the toxic strip came from recently
glazed structures. The manufacturers confirmed that a change in formulation of the glazing
strip had occurred in 1981. Of the several cases now known, in which similar disorders have
been found in monocrop tomatoes, all were in recently erected or reglazed glasshouses and
new glazing strip had been used. At NVRS a new glasshouse was being used to raise Brassica
species and these plants were abnormal even in early autumn, when ventilation was
occurring. Discussions with the glasshouse manufacturers and their suppliers of glazing strip,
together with collaborators from ICI, led to the recommendation that the toxic glazing strip
should be replaced by strip containing only DIDP as plasticiser. We tested the new
formulation in our bioassay and found it to be non-toxic. An additional change was
incorporated into this new strip in that the original aluminium powder which gave a silvery
appearance to the glazing strip was replaced with carbon black. This was likely to improve
the stability of the material and it made the new glazing strip conspicuously different from the
original. It should be emphasized that only the recently manufactured batches of the silvery
glazing strip might be toxic.
Comparison of the three types of glazing strip in a radish bioassay is shown in Fig. 4. It is
obvious that the strips containing DEHP or DIDP were innocuous but the strip which
included DIBP was very toxic. The remaining three plants after 10 d treatment are shown in
Plate 1.
In addition to the favourable bioassay for the new, black glazing strip it was also necessary
to have long term tests under commercial conditions. One such test was at NVRS in which
two of the five sections of the experimental glasshouse had the old glazing strip replaced
whereas the other three did not. The two renewed sections have now shown no disorders for
more than a year whereas in the sections containing the original strip, brassicas still produced
the standard chlorotic syndrome (Hardwick, Cole, and Fyfield, 1984).
Value of losses in monocrop tomatoes
Investigation of the commercial implications was made possible by the kind cooperation
of the tomato nursery in which we first diagnosed the toxic glazing strip in the new
glasshouse. This nursery also had similar glasshouses with non-toxic glazing strip. The
nurserymen kept records of yields in the two comparable houses from the winter of 1981
when the new, toxic house first came into use. In the autumn of 1983 the toxic glazing strip
was replaced with the non-toxic black strip. The yield comparisons for 1983 and 1984 seasons
are shown in Table 2.

Hannay and Millarâ??Phytotoxicity of Phthalate Plasticisers 891
TABLE 2. Calculations for loss in gross crop value due to toxicity from glazing strip
Year and month
1983 March
April
May
June
July
August
September
October
Annual totals
1984 March
April
May
June
July
August
September
October
Annual totals
Average
value"
(£ ton"1)
1199
1180
886
697
683
503
332
427
1069
1107
1075
629
726
623
298
498
Toxic House
Yield
(ton acre"1)
1-3
9-8
19-9
26-8
318
23-7
17-5
121
142 9
9-5
16-8
21-4
28-8
283
22 1
14-0
18-9
159-9
Crop value
(f month"1)
(A)
1559
11564
17631
18680
21719
11921
5810
5 167
£94051
10156
18 598
23005
18115
20546
13768
4 172
9412
£117772
Control
Yield
(ton acre"1)
41
17-6
24-7
29-4
31-8
23-8
19-9
172
168-5
9-2
191
24 5
287
25-3
20-2
12 4
16-1
155 7
Crop value
(£ month"1)
(B)
4916
20768
21884
20492
21719
11971
6607
7344
£115 701
9835
21 144
26338
18052
18368
12 585
3 695
8018
£118035
Monthly loss
(gain) in crop
value £
(B-A)
3 357
9204
4 253
1812
_
50
797
2177
£21650
(321)
2546
3 333
(63)
(2178)
(1 183)
(477)
(1394)
£263
* Data for mean monthly crop values from ADAS, South Coast Glasshouse and Mushroom Advisory UniL,
Chichesten baled on gross returns for Class 1 tomatoes.
The glazing strip in the Control contained only Di-octyl phthalate as plasticiser and was assumed to be non-toxic.
The glazing strip in the TOXJC house contained Di-octyl phthalate plus Di-isobutyl phthalate during 1983 but in
November 1983 this was replaced by glazing strip containing only Di-isodecyl phthalale as plasticiser.
Each house was about one third of an acre but they were not identical in size. All the plants
were grown by nutrient film technique.
The main points to notice are:
(a) The loss in yield in 1983 occurred mainly in the first three months but also in
September and October.
(b) Because the price of tomatoes varies with the time of season, the financial loss was
relatively greater than the loss in yield.
(c) In 1984 there was virtually no difference in yield, or crop value, between the original
glasshouse and that in which the toxic glazing strip had been replaced.
Circumstances affecting the overall picture were:
(i) In 1983 all the young plants were kept for 8 weeks in the 'toxic' house, from
mid-October to mid-December, until they were planted out into their final positions.
Thus even the 'controls' would be partially retarded and, therefore, will have caused an
underestimate of the relative damage.
(ii) In 1984 the reglazed house had a fairly serious root infection from Phytophthera in
March and April which probably depressed yields temporarily, whilst in July the
'control' house was infected with whitefly which would depress yields till the end of the
season.
In spite of these vagaries, the figures provide a good approximation to the sort of losses
that can occur. In 1982 the loss was around £22000 per acre in the toxic house but some of
this was due to differences in planting dates since the new house was not ready until

FIG. 5. The effects of dibutyl phthalate, either alone or incorporated into PVC, on photosynthesis and
respiration in radish shoots. Each point above the axis (photosynthesis) is the mean value during the 18 h
photoperiod and those below the axis (respiration) are the mean values for the 6 h dark period.
December 1981. In 1985, up to the end of August, the 'loss' was about £2000 on the reglazed
house but the monthly yields are variable and the 'loss' may well be within the normal limits
of variation between houses. The problem may be confined to tomato crops in the winter and
early spring when the glasshouse is almost sealed to retain heat and to facilitate carbon
dioxide enrichment of the atmosphere. Once free ventilation occurs the toxin level falls and
the tomatoes grow well.
Toxicity due to inhibition of photosynthesis
In an attempt to discover the reason for the toxicity of the phthalates, whole shoots of
radish plants were enclosed in small individual growth chambers, so that the change in
carbon dioxide concentration of the air passing over each shoot could be monitored.
Photosynthesis in treated plants was inhibited but there was virtually no effect on respiration
(Fig. 5).
The data are from only three individual plants but the trend shown is typical of several
experiments. The plants were of different sizes at the end of 10 d but this was compensated
for by using unit leaf area for comparison. This does not allow for the presence of
chlorotic patches on some leaves of the treated plants, so a decrease in photosynthesis
was not surprising; a more useful comparison may have been on a unit chlorophyll
basis. Nevertheless, under these circumstances the respiratory process was not seriously
affected; it appears much less sensitive to the toxic phthalates than the photosynthetic

Hannay and Millarâ??Phytotoxicity of Phthalate Plasticisers 893
Measurements were also made of the stomatal resistance of each plant at the beginning
and end of the 10 d enclosure in the IRGA system. Table 3 shows the results. In all treatments
the stomatal resistance was lower at the end of the experiment than at the beginning but there
was no obvious difference between the three treatments. The decrease in photosynthesis does
not appear to be due to stomatal closure effected by DBP.
TABLE 3. Total leaf areas and stomatal resistances at the start and end of CO2 exchange
measurements
Mean of three leaves ±s.e.
Treatment
1. control
start 2. DBP plastic
3. DBP plasticiser
1. control
end 2. DBP plastic
3. DBP plasticiser
Leaf area
(cm2)
39-5
450
43-75
73-6
50-00
55-10
Stomatal
resistance
(±s.e.)(s m"1)
7-3 ±0-84
6 9± 1 16
8-2±l-75
2-4 ±0-01
21 ±0-36
2-9 ±0-45
Chloroplast development disrupted
Investigations of the fine structure of treated leaves, in 1979-80, by third year
undergraduates revealed that chloroplast development in the youngest chlorotic leaves,
which had developed during exposure to phthalates, was severely disrupted. There were few
grana. The treated leaves also had increased numbers of plastoglobuli but starch grains were
absent.
These early, unreplicated observations have been confirmed and extended to an
examination of the effects of butyl phthalates on the more mature leaves, which were already
green and fully expanded when the exposure to DBP was commenced. These leaves normally
remain green during a 10 d exposure in the bioassay even though the younger leaves are
chlorotic. Plate 2 shows four photomicrographs to illustrate these observations. The upper
two photographs (A and B) show the comparison between a control and a treated young leaf
and the lower photographs (C and D) compare control and treated mature leaves. The
immature leaves show the typical lack of development of grana, as found previously, but the
mature leaves have well developed grana, though they have never been found to include any
starch grains when sampled after 5 d exposure to DBP. The obvious effect in the mature
chloroplast is the swelling which causes the normal ovoid shape to round out and the
thylakoid system to be pushed towards the vacuole. Plastoglobuli also appear to be more
numerous but there is no obvious breakdown of the thylakoids.
From these observations it is not surprising that photosynthesis is inhibited in
DBP-treated leaves but it is not clear whether the inhibition is equally severe in the young
versus the mature leaves. Mitochondria appeared normal in sections of DBP-treated leaves.
This is consistent with the absence of inhibition of respiration. Virgin, Hoist, and Morner
(1981) also remarked that mitochondria in young leaves appeared to be unaffected by an
exposure to DBP which completely disrupted the chloroplasts.

PLATE 2. Photomicrographs of sections through radish leaves to show chloroplasts from: (A) a young
radish leaf ( x 18 000); (B) a young radish leaf exposed to DBP vapour for 3 d ( x 18 000); (C) a mature
radish leaf (x 26000); (D) a mature leaf exposed to DBP vapour for 5 d (x 26000). Gâ??granum;
Thâ??thylakoid; PGâ??plastoglobuli; SGâ??starch grain; Mâ??mitochondrion; NAâ??nucleic acid (DNA);
Sâ??stroma; CEâ??chloroplast envelope; Vâ??vacuole.
DISCUSSION
In September 1981, a computer search of the literature revealed nothing about PVC toxicity
to plants. At that time it was not known that phthalates were involved and this keyword was
not used. Since then many important references have turned up (see Millar, 1985 for full
bibliography). The most relevant came from personal enquiries to Japanese and German
scientists. In the early 1970's important investigations into phthalate toxicity in PVC film had
clearly established that the butyl phthalates were the cause. Unfortunately records of these
investigations were relatively inaccessible in bulletins of research stations, or even in
advertising literature. In view of the importance of PVC film in horticulture in Japan, which
uses over a quarter of a million tons of plasticised PVC film annually (Dubois, 1978), it is
surprising that the manufacturers in the U.K. had not sought the reason why it was not being
used here. There is no reason to castigate the manufacturer who included DIBP in the glazing

Hannay and Millarâ??Phytotoxicity of Phthalate Plasticisers 895
strip formulation. Butyl phthalates are still listed as satisfactory for food-grade film. Any
enquiries made in this country in 1980-81 would have been unlikely to have raised any
objection to the use of DIBP. Similar errors have been made previously, in Germany and
Japan. There is no reference to PVC toxicity to plants in the book 'Plastics in Agriculture'
(Dubois, 1978). To alert the horticultural industry to the cause and cures of the glazing strip
problems, a note was published anonymously in the Grower (Anon, 1983).
The commercial data on tomato crops shows that the toxic glazing strip can cause serious
losses of around £20 000 per acre per year. The cure is expensive because it is a skilled and
time consuming job to replace the glazing strip. Apart from glazing strip other glasshouse
equipment such as hose-pipes and trickle irrigation systems could be a hazard though only a
few cases are known. Most of the glazing strip and trickle irrigation problems are likely to be
confined to PVC made during mid-1981 to mid-1983. Anything purchased since then should
contain no butyl phthalates because all plastics manufacturers were informed of the problem
in summer 1983. However, hose-pipes and paints might still be problematical. Different
species show varying sensitivity to the toxic phthalates. Brassicas are particularly sensitive
and are useful for bioassays. Other crucifers such as alyssum (Lobularia maritima L.) and
ten-week stock {Mathiola incana L.) are also sensitive. Tomato is less sensitive than the
brassicas but lettuce will grow well when tomato and brassicas are badly damaged; rye grass
(Lolium perenne L.) is also very resistant. It is probable that most plants are fairly resistant but
Virgin et al. (1981) reported that some house plants were affected by butyl phthalates
volatilizing from paint in newly decorated rooms. Hardwick et al. (1984) reports significant
differences in sensitivity between different cultivars of cabbage. More work needs to be done
to screen glasshouse plants for sensitivity. There may be other species among bedding plants
and house plants which are susceptible, but this may not be diagnosed correctly if most other
species growing alongside them appear to be healthy.
It is still unknown why some plants are susceptible when others are resistant but it is
important to discover the reason. Then it may be possible to combat toxicity in susceptible
plants, or even to turn the differences in sensitivity to advantage as a basis for a herbicide.
Only the butyl phthalates are phytotoxic under commercial horticultural conditions and
in our bioassay. The bioassay produces the toxic syndrome within a few days and young
seedlings die within 2 weeks of exposure to atmospheric concentrations in the region of
160-180 ng dm " 3 of DBP or DIBP with an air flow of 30 dm3 min " ' (this gave about one air
change every 5 min in the growth chamber). Hardwick et al. (1984) reported a maximum
concentration of butyl phthalates in the affected glasshouse at NVRS of approximately 2-0 ng
dm ~3 (average 1 -2 ng dm "3) which is about a hundred times lower than that measured in the
bioassay. At that concentration many brassicas could not be grown satisfactorily. The
concentration dropped to around 10 ng dm"3 during ventilation in late summer; brassicas
did not grow satisfactorily even at this reduced level. No symptoms were visible when the
detected concentration was lower than 014 ng dm"3. Presumably the concentrations of
phthalate in the tomato nursery were higher than 2-0 ng dm"3 DIBP during the
non-ventilated winter period when the plants were affected. No measurements were made at
this time because the analytical technique was not developed until 1984.
At the concentrations present in glasshouses during wintertime, young tomato plants need
about 3 weeks exposure before a trained eye can spot the first signs of disorder (N. Starkey,
personal communication). With a prolonged exposure of three months (December to
February) symptoms are severe. The young leaves have a yellow-green interveinal mottling
but not an obvious chlorosis; the old leaves have quite large blotches of interveinal necrosis
and at worst the necrotic patch goes completely white or transparent and may be 2-3 cm2 in
area. Only about half to two thirds of the leaf is green; the rest is papery and with occasional

896 Hannay and Millarâ??Phytotoxicity of Phthalate Plasticisers
transparent patches. Nevertheless, the first truss sets but the fruits are smaller and fewer in
number. This also happens in the next few trusses and even when ventilation commences it
may take another 2 months or so before the plants produce a near normal crop. They do not
make up the early losses and towards the end of the season, when ventilation is reduced, they
again show a small decrease in yield.
The cytological changes of chloroplast structure seen in the electron micrographs are
consistent with those found by Virgin et al. (1981) so far as the young leaves are concerned.
Virgin et al. (1981) showed no pictures of mature leaves following treatment but implied that
such leaves also became chlorotic. This was not so during the fairly short exposure time given
in our bioassay, although it produced severe chlorosis in the young leaves. The mature leaves
showed no chlorosis and no malformation of thylakoids or grana. However, the whole granal
system was displaced towards the vacuole. This visual evidence suggested that the
chloroplasts could be capable of carrying out photosynthesis in the mature leaves but not in
the young leaves. Virgin et al. (1981) also found a marked decrease in carotenes in young
treated leaves and an accumulation of a carotene precursorâ??probably phytoene. They
suggested that the mechanism of action of DBP could be interference with carotene
metabolism. Thus, free radicals generated by chlorophylls during photosynthesis would
not be quenched and bleaching would result in chlorosis. If this hypothesis is correct, yet
mature green leaves do not become chlorotic during treatment, then carotene turnover in
mature leaves must be negligible. The carotene formed in the young leaf, prior to exposure
to the toxin, must continue to act as a quenching agent. After several weeks exposure of older
plants we occasionally do find mature green leaves which start to turn chlorotic. This may
be due to enhanced senescence rather than a direct effect of the phthalates on carotene
synthesis.
ACKNOWLEDGEMENTS
The authors' wish to thank the SERC and ICI for a CASE studentship (DJ.M.) and the latter
for chemical analysis of plastics; undergraduates for assistance with EM work (D. Moss, C.
Mallory and A. Waite); and to V.M.C. Baileys and partners for providing data on their
tomato yields.
LITERATURE CITED
ANON (Undated). Plasticised PVC in Horticulture. Report on BASF plasticisers. BASF, Ludwigshafen,
Germany.
ANON, 1983. New glazing strip damages glass crops. Grower, 23 June, pp. 5.
AUTTAN, J., 1973. Toxicity and health threats of phthalate esters: review of the literature. Environmental
Health Perspectives, 4, 3-26.
CROSBY, D. G., and SINGMASTER III, J. A., 1973. Phthalate esters as artifacts in pesticide research.
Abstracts of Papersâ??American Chemical Society 166th Meetingâ??Pesticide Chemistry, p. 59.
DUBOIS, P., 1978. Plastics in agriculture translated from the French edition (1973) and revised by C. A.
Brighton. Applied Science Publishers, London.
GIAM, C. S., CHAN, H. S., and NEFF, G. S., 1975a Sensitive method for determination of phthalate
plasticisers in open ocean biota samples. Analytical Chemistry, 47, 2225-9.
19756. Rapid and inexpensive method for detection of polychlorinated biphenyls and
phthalates in air. Ibid. 47, 2319-20.
GLAUERT, A. M., 1980. Fixation, dehydration and embedding of biological specimens. In Practical
methods in electron microscopy. Volume 3. Ed. A. M. Glauert. North-Holland, Amsterdam.
Pp. 1-201.
GROSS, F. C, and COLONY, J. A., 1973. The ubiquitous nature and objectionable characteristics of
phthalate esters in aerospace technology. Environmental Health Perspectives, 3, 37-47.
Hannay and Millarâ??Phytotoxicity of Phthalate Plasticisers 897
HANNAY, J. W., 1980. Fumes from flexible PVC damage young plants. Grower, 21 August,
Pp. 28-9.
HARDWICK, R. C, COLE, R. A., and FYFIELD, T. P., 1984. Injury to and death of cabbage (Brassica
oleracea) seedlings caused by vapours of dibutyl phthalate emitted from certain plastics. Annals of
Applied Biology, 105, 97-105.
INDEN, T., and TACHIBANA, S., 1975. Damage of crops by gases from the plastic materials under
covering conditions. Bulletin of Mie University, Faculty of Agriculture, 50(6), 1-10.
MILLAR, D. J., 1985. Phytotoxicity of phthalate plasticisers. Ph.D. Thesis, University of London.
SEARS, J. K., and DARBY, J. R., 1982. The technology of plasticizers. Wiley-Interscience, New York.
VIRGIN, H. I., HOLST, A. M., and MORNER, J., 1981. Effect of di-n-butylphthalate on the carotenoid
synthesis in green plants. Physiologia plantarum, 53, 158-63.

Could you give a bit more detail please?

[bigsby]

When a company sells a product under their brand, they are liable for any negative outcomes. It does not matter who produces the inputs to that product, it is the responsibility of the representing company to perform due diligence on their products. If the suit is successful, the representing company can seek relief by suing the supplier of the faulty input, but that is secondary to this discussion. u.g.u is right.

[u.g.u]

RECOVERY METHODS

Just so everyone knows how to make recovery as fast as possible. 1st remove every last bit of tube 2nd reduce light it is phytotoxic so light reacts and causes the burn. Either move the plants out from direct light or put a piece of window screen over the lens of the hood to cut the light output. 3rd is foliar feed I did a 300ppm of my base nutes a couple times a week. 4th cut co2 and just use air your plants cannot benifit from co2 when they are in this condition. 5th if you have a carbon filter turn it on the carbon traps any molecules floating around. 6th wouldn't be a bad idea to do a res change it is a low molecular wieght phthalate so it is soluble in water according to some research I found last night.

[u.g.u]

So I had a meeting with my lawyer today we decieded to proceed with the case. Even though they threatened us with FEDERAL LAW. whatever this is about proving a point. DON'T SELL TOXIC PRODUCTS.

[Prodaytrader]

As far as I know you can sue anyone, for anything, at any time. That's the general rule anyway. The second general rule is to sue everyone in the chain from the guy who you first talked to in the store all the way to the guy who invented the product, up to and including: sales, retailers, wholesalers, distributors, manufacturers, and if possible the material suppliers as well. Once all the suits are filed, you let the judge and jury sort out who is at fault.

From what I can tell you are very angry about what has happened to you and your looking for someone to take accountability. That likely wont happen especially when dealing with Chinese firms. I did see that somewhere right, that the tube was made in China?

[u.g.u]

Prodaytrader
Ya its made in china That is why I went after NGW(Not Grow Worthy) and not the actual manufacture. Plus it has NGW's name on it. My lawyer basicly said the same thing as you. We decided not to go after the retail store for 1 they really had no Idea and 2 it was one of my good friends. Also a suit like this would more than likely shut down a small store they would just file BK and nobody would get anything.

[u.g.u]

Late night horror stories
Man, this is some bullshit... I'm pretty damned sure that this has been my problem all along... I've been thinking for months and months that I'm retarded and just can't "get" hydro... I've been listening to everything that everyone has been telling me, I've tried half strength nutes, I've tried distancing the light a whole shitload (36"+), different nutes, etc and nothing seemed to work.... I am using those damned N-G-W tubes too man..... Fuck these bastards! Let's get this class action going. They can't be selling hydroponic hose that releases toxins into the water, that shit is ridiculous!

i think i ran into this last fall when i set up the hydro at my newest location. i ended up taking them out of hydro, set them in dirt and they all survived..... HHB

OMG! Are you talkin bout this dammm shitbag blue-ass fukkin crap in this picture>?!?!?!?!? Notice any telltale clues in the backround?

I got a 100 foot roll of this in january and have gotten 2 ounces total since then running 1000 watts in a 4x4 RDWC. What the hell other brand are we suppose to get then?

Ack...just checked my tubing cuz the name stamp on the tubing rang a bell. Sure nuff...
I had offgassing probs identical to those pics about 2 years ago w/ Hydrohuts. I had a 4x8 and a 3x3 Hydrohut in my room and it put me out of business
I'm gonna change out all my tubing tomorrow. Why do I always buy lemon products (sigh)?

just went and got 100' roll of hydrofarm black 1/2", that should be safe. My buddy that set me up in january has 10 years under his belt and he is using mostly the black hydrofarm but he got a roll of blue shit the same time I got mine, he said in the area where he has it in his bigger room he has some yellowing leaves also he is ripping it out tonight. 2nite the second the lights come on its rip the blue shit back and store it in the garage

I had identical problems in a new space i setup last january... Tried forever to figure it out looked at all the variables... After 3 harvests that barely yielded 25% of what they could have i gave in and moved the room to another area of the house where I had a veg space that was unaffected.. Thankfully it solved my problem cuz i was bleeding money fast and about to have to take a huge loss.

Ill check and c if the tubing i used is the same as yours... I never changed my tubing when i switched rooms tho... Your leaf problem is identical to what we had goin on... We were convinced it was ethylene for awhile. We never actually figured it out...

It also looked like Snoopytimes pics...
Are u sure it was the tubing? I thought I had it figured out a bunch of times only to have it continue. I'll dig up some pics of our damaged leaves.

Fuck me.
I've been running that same blue 1/2 tube for the last eight months and I've lost every fucking crop.
I've wasted everything I had trying to diagnose what the hell is going on... The only thing I didn't change out was this crap hose.
Fuck me.
No, wait:
Fuck them.
EDIT: I just went back through my last grow. My roots started to discolor the day I added my auto-top off reservoir. And I connected it to the system using this shit hose.
And the same hose is attached to my system right now.
EDIT: Two hours later, it is no longer in circulation. Thanks for the heads up UGU.
I got rid of all of my oldest pics from the first grow with this tube, but they all had the same shitty yellowing. I thought it was N, then I thought it was mag, then I thought it was lockout, then I thought it was root rot/slime. If I just wasted the last eight months on toxic tube...

On the upside: maybe I'm not such a shite gardener after all....
Omfg dude. I've been using this tubing and have lost countless harvests. Some of it was aphids, but I'm almost positive this is why my 3kw room experienced spontaneous death.
Good fuckin' work, bro. You deserve a medal. I'm gonna call my local hydroponics store and demand that they stop stocking this shit.

those pics are exactly what we experienced UGU makes me shudder....
Turns out the tubing in my room is the same stuff...

Yeah man i have the blue, and like I said I had 9 months in a row of bad grows . . well non-grows really. It was crazy, you put a healthy begged out plant in there and after a week the leaves start getting interveinal chlorosis as in calmag deficiency. I tried using 1/2 tap water, adding calmag first, last, topping off with it etc. then the leave die.
My latest theory since I had root problems as well was that root rot lowered my PH to where they couldnt get any phosphorous. But now that I did a wack dose of Physan followed with hydrofungicide my roots are white as a $30,000 set of teeth lol. So yeah the blue stuff officially sucks too.

THANK YOU SO MUCH
I run a RDWC system with NGW hoses, I have ran the system for over a year. I have never once had any signs of this off-gassing happening.
Although...
I setup my friend with a RDWC system with this hose. Every parameter was perfect the whole time, but we could not figure out why his plants looked like shit. It boggled my brain, and I had accepted he had some "nasties" in the system. (IE: not cleaned or maint. well)
He lost two crops in a row, his first two in this sytem. Prior to those grows he had successful harvest in single chamber DWC, and the two new grows he had much more equipment to be successful, it just didn't make sense.
Well today it did, the pictures and information displayed here are exactly what his problem
was. He here now checking it out, lifting his spirits about his defeated grow.
So why is it my 100+ foot of it in my system (the black 1/2") is fine while his 1/2" black hose wasn't.....
I called my local shop and I am attaching this information to an email for them to check out. This hose is literally putting people under from what I have seen, and it can't happen to anyone else.
FUCK NGW there business in the grow industry is OVER!!!!!
Tell all your shops all your friends, make sure they remove this SHIT hose!!! Lets make an example of them!!!!
Ok I went and checked my hose, I am using hydrofarm hose with great success. My friend did infact have NGW feedhose and it did kill his only to crops in RDWC. It looks identical to all the pictures shown here.
edit: This must be stickied before anyone else loses their crop.


Wow... Pretty sure I lost three whole crops, a car, best friend and almost everything else worth of value that I owned because of this issue...
A friend of mine built a DIY ebb n grow-type bucket system for me when I first started out. He had used the same exact system before with great results. For some reason I couldn't, for the life of me figure out why my plants kept instantly dying off (it was my first time ever growing so I had no clue of what was what). I'd blame it on heat, light intensity, root rot, phosphorus def., you name it. When I saw the pics from this thread I couldn't help but notice my plants looked exactly the same. Just so happens that all the tubing used had ngw.com stamped all over it. I think this is far from a coincidence....

Yes Bro your story is almost exactly mine. My pal set me up, same everything (we thought) as him. All year long he hauled in monster buds the size of kid footballs, while I was getting 2 foot skinny dried up sticks with yellow wispy dried out leaves on top. This pal of mine has around 10 years doing it and perfected his system along the way, so he kept asking me "ARE YOU SNEAKING AND PUTTING FOO-FOO SHIT IN THERE!?!?!?!" . . "HOW MANY TIMES A DAY YOU FUCK WITH THEM?!?!?!?"

I blamed it on exactly every same thing you did. (You left out cal-mag def lol.) When it first comes on it looks like magnesium deficiency, the in between veins become light green first. Then it spreads to the whole leaf and the edges start crackling yellow at the tip and progress all the way to the petiole. In fact, the second pic in Phosphorous deficiency here: https://www.icmag.com/ic/showthread.php?t=11688

had me believing that root rot dropped my PH and they couldnt get any so I was PH UPping the shit out of them.

Well now that it has been a solid 5 days with NO NGW.COM tube in my room, I can safely report that there is NO FURTHER YELLOWING! In that room I have plants toasted that have been in there 6 weeks, they have no leaves and the buds are the size of SERIOUSLY a piece of popcorn each. THen I have one thats been in there 2 weeks that was rocketing up and stretching then started pale greening by the time I changed the hose. THat one isnt getting any worse, its still all 'green' but its frozen - no new growth. Its seriously stuck in a time warp.

Then I got 2 plants that have been in there for around 8 days, so they got around 3-4 days of poisoning. they arent yellowing or fading, but the new growth is pale and it seems like they are at least semi frozen.
Then I got 1 that I put in an hour after the hose got changed. It has fresh new growth, however it is not rocketing because I put it in there from veg pre-maturely as a sacrifice test. Its roots were a little screwy since my veg station had only recently been light proofed. But still, I am 90% confident that my most serious problem has been rectified.
In my opinion, the boss of this site should spam this thread out to EVERY member. I reallllly cant see anyone from this community getting annoyed about getting an email that *MIGHT* save their closet career.

Same Story for my friend, I set him identical to my successful system, and his plants were the worst crops I have ever seen. The two crops he spent 4-6 months loosing set him back, to not growing, no job, lost unemployment, and behind in bills. He was happy to learn of the cause yesturday, and so was I. I felt so bad I couldn't solve his problem. His life would be exactly oppisite right now if it wasn't for that hose. I estimate 20K lost

son-of-a-biii-otch!! I spent 500$ on hose an cut all shit up. Now I got that same problem. And it is the ngw crap. After this run i'm changing it all out. thanks for the heads up, now i can stop bitching.

Fuck

This explains the declining condition of my mothers since I moved them into the hydro veg area. Looks exactly like the pictures. I couldn't figure out why super healthy mothers suddenly went into decline.
Looks like im changing out 200'+ of this shit, in little 10"-12" pieces. I know what I'm doing this whole freaking weekend.
Thanks for the diligence! You may have saved more people than you realize.
Maybe it was a DEA ploy to kill off the industry.... The plot thickens.

I have been frustrated to the point of seriously considering just shutting down for a while due to this until I found this thread. Same story as everyone else, chased all these phantom issues for months and nothing ever helped. Before seeing this thread, I recently switched out my black 1/2" ngw tubing for some of their white. Interestingly enough, there was no ngw markings at all. The two types of tube also smelled noticeibly different with the white being the typical plastic smell while the black was very strong burnt rubberish. I only had the white stuff in there for a few days until I found this, my plants were still yellowing so I'm assuming the white stuff is bad too. At this point I'm ripping every inch of the shit out just to be safe.

Jeez, look familiar? Two years of this shit. Thanks U.G.U Never considered the damn tubing.

Add another system to the count guys, PTB's RDWC fuckin' died....nice.

I witnessed PTB's myself. 1 more week of flushing and the shit was a wrap. He started treating with cal-mag a couple weeks ago. The NGW hose killed off his roots, and as of last night they gave up. 12 buckets with beautiful full lush ladies......
NGW is literally fucking up grow after grow....do not think that it won't happen to you. remove this shit ASAP.
I have seen 3 RDWC grows fall flat on their face now from this hose. It seems in this system, it turns the roots to mush/rot. In 68F pure RO water.....heavily oxygenated, controlled sealed environment. Strain we have both worked for years...
Yea chalk another one up to off gassing... im totally pissed... rooms numbers all spot on 1/4 chiller water temps stay at 68.....
Roots TOTAL MUSH!!!!! got the cal mag deffiecency look about 2 weeks ago... started treating for calmag... plants where totally fine last night and then this morning everything was all droopy dead dieing.. check hose... NWG.com!!!
Called PK over cause hes seen offgassing before with his cousin... says looked exactly the same... do not know whats up but very salty.... what im wondering is how some poeple shit dies instantly and some like mine too months to finally show though i do believe it never let the roots actually take hold... they alwyas looked ruff....

My plants started going to hell about three weeks into veg this time around.

lol just as an off note . . anyone who has suffered through this probably had similar crazy thoughts. But SERIOUSLY, I would look at my depressing shit, then come to ICMAG to try and find an answer. . . I would see threads like "20k Big Dog Roadshow" . . "8k watts MPB" / . . .etc . , , and think to myself "WHAT THE FUCK AM I DOING WRONG! How are these guys using 20 lights at 1000 watts each and mine turn yellow with 1 light 4 feet away set on 600!?!?!??! It reallllly made me think I was going nuts

NGWNOT GROW WORTHY

[u.g.u]

So my buddy that owns a shop in town called NGW today and asked them about returning his inventory of tube. And what they were planning on doing about it. Their response was they had the tube tested by an expert and found it was not toxic enough to kill plants. So they will continue selling the tube. He told them that he can personly atest for at least 30 rooms that he also saw with his own eyes. The guy really had nothing to say at that point. Even said fuck those guys they going to loose in court. Bring it on assholes.