Last night I shelled seven hips from Margaret Merrill, and have lots of seeds. I live in So. Cal. Do I actually have to buy a 5lb bag of Captan to prevent them moulding? Could I just put them in some peat in a plastic bag in the crisper? Please, I would appreciate any instructions because I misplaced my little hybridizers handbook, - I know, I know… but I have two small children so the pamphlet could be anywhere, and of course I had to jump the gun and open up those hips!! How long can I leave them in a plastic cup on my windowsill? (I still have quite a few more hips I can harvest, fortunately)
Thanking y’all in advance
Andrea McCullough
I have always been able to find Captan 50% WP in the 12 oz. cardboard can. I purchased some last week at a local farm supply. I think the 5 lb. bags are for the commercial user. Good Luck
It’s not at all necessary to buy captan. If you have some peroxide like is used to treat wounds, or household chlorine bleach you can achieve the same thing.
use peroxide full strength(3%) or mix a couple capfulls of bleach to a quart of water, and soak the seeds for a few hours before putting to your moist peat for stratification.
Some people don’t treat the seeds with anything at all and get germinations, but I have learned from experience that it’s nicer to work with seeds that haven’t gotten all moldy.
There are some types of mold that may actually enhance germination, but unless you know what kind the mold is you could end up ruining some seeds if they mold. Having said that…I still would try any seeds that get moldy. I have had success with them in the past, but usually they don’t have as high of germination rate if they get too badly infected.
Advice is worth what you pay for it, so take all this with a grain of salt and don’t be afraid to try some of your own methods.
Good luck,
Randy
Captan will work, but so will a soak on H2O2. Captan, by the way, is a proven carcinogen, and you should NEVER put it in a fridge that you use for food.
For the past 2 years I have stored my seeds in well washed sand, dampened and in sandwich bags, then placed in the fridge. I use no fungicides in the damp sand, and have little or no fungus problems.
Paul
FWIW, here’s information/non-information re. captan’s classification as a carcinogen/potential/probable/non- carcinogen. Take your choice: it is/maybe is/is not a carcinogen.
Cancer: No information is available on the carcinogenic effects of captan in humans. One strain of mice orally exposed to captan reportedly developed tumors of the duodenum.
The U.S. EPA has classified captan in Group B2: Probable human carcinogen (U.S. EPA, 1994a).
The International Agency for Research on Cancer has classified captan in Group 3: Not classifiable as a carcinogen (IARC. 1987a).
The State of California has determined under Proposition 65 that captan is a carcinogen(CCR, 1996). The inhalation potency factor that has been used as a basis for regulatory action in California is 6.6 x 10 (microgram per cubic meter) (OEHHA, 1994). In other words, the potential excess cancer risk for a person exposed over a lifetime to 1 g/m of captan is estimated to be no greater than 0.66 in 1 million. The oral potency factor that has been used as a basis for regulatory action in California is 2.3 x 10 (milligram per kilogram per day) (OEHHA, 1994).
Link: www.arb.ca.gov/toxics/tac/factshts/captan.pdf
An official “position” normally lags the published scientific research.
Authors: McDuffie, Helen H.; Pahwa, Punam; McLaughlin, John R.; Spinelli, John J.; Fincham, Shirley; Dosman, James A.; Robson, Diane; Skinnider, Leo F.; Choi, Norman W.
Title: Non-Hodgkin’s lymphoma and specific pesticide exposure in men: Cross-Canada study of pesticides and health.
Journal: Cancer Epidemiology Biomarkers & Prevention, Volumn 10, pages 1155-1163, (2001).
Abstract: "Our objective in the study was to investigate the putative associations of specific pesticides with non-Hodgkin’s Lymphoma (NHL; International Classification of Diseases, version 9 (ICD-9) 200, 202). We conducted a Canadian multicenter population-based incident, case (n = 517)-control (n = 1506) study among men in a diversity of occupations using an initial postal questionnaire followed by a telephone interview for those reporting pesticide exposure of 10 h/year or more, and a 15% random sample of the remainder. Adjusted odds ratios (ORs) were computed using conditional logistic regression stratified by the matching variables of age and province of residence, and subsequently adjusted for statistically significant medical variable (history of measles, mumps, cancer, allergy desensitization treatment, and a positive history of cancer in first-degree relatives).
See next post for the rest of abstract.
Part 2 of abstract.
We found that among major chemical classes of herbicides, the risk of NHL was statistically significantly increased by exposure to phenoxyherbicides (OR, 1.38; 95% confidence interval (CI), 1.06-1.81) and to dicamba (OR, 1.88; 95% CI, 1.32-2.68). Exposure to carbamate (OR, 1.92; 95% CI, 1.22-3.04) and to organophosphorus insecticides (OR, 1.73; 95% CI, 1.27-2.36), amide fungicides, and the fumigant carbon tetrachloride (OR, 2.42; 95% CI, 1.19-5.14) statistically significantly increased risk. Among individual compounds, in multivariate analyses, the risk of NHL was statistically significantly increased by exposure to the herbicides, 2,4-dichlorophenoxyacetic acid (2,4-D; OR, 1.32; 95% CI, 1.01-1.73), mecoprop (OR, 2.33; 95% CI, 1.58-3.44), and dicamba (OR, 1.68; 95% CI, 1.00-2.81); to the insecticides malathion (OR, 1.83; 95% CI, 1.31-2.55), 1,1,1-trichloro-2,2-bis (4-chlorophenyl) ethane (DDT), carbaryl (OR, 2.11; 95% CI, 1.21-3.69), aldrin, and lindane; and to the fungicides captan and sulfur compounds.
Still too long see part 3 for rest of abstract.
Part 3 of abstract.
In additional multivariate models, which included exposure to other major chemical classes or individual pesticides, personal antecedent cancer, a history of cancer among first-degree relatives, and exposure to mixtures containing dicamba (OR, 1.96; 95% CI, 1.40-2.75) or to mecoprop (OR, 2.22; 95% CI, 1.49-3.29) and to aldrin (OR, 3.42; 95% CI, 1.18-9.95) were significant independent predictors of an increased risk for NHL, whereas a personal history of measles and of allergy desensitization treatments lowered the risk. We concluded that NHL was associated with specific pesticides after adjustment for other independent predictors."
End of abstract.
Henry,
Did you find any numbers to indicate how much the researchers think the increased risk is for the captan and sulfur compounds?
Peter, that was the complete abstract. I do not have the actual paper.
Looks like very low numbers on the increased risk posed by captan and the sulfur compounds. I’m not surprised by the higher numbers for risk on some of the other pesticides and fungicides. Less than one in a million for a lifetime of exposure is not much of an increased risk–if the California numbers have any validity. Sometimes I wonder how valid the numbers are, and what the increased risk of cancer would be to one who spends too much time looking at those numbers on a computer screen. Where I live, pollution from autos, factories and coal-fired power plants (and my lawn mower) is probably a far greater risk than that posed by my fungicide use. Just to keep things in perspective…
Peter: “Looks like very low numbers on the increased risk posed by captan and the sulfur compounds.”
I do not interpret that the fact that numbers not being quoted in an abstract indicates anything about their magnitude (is this a proper sentence).
The Journal (and Editor) often restrict the size of an abstract. Not everyting can be put into it.
Author: Mills, Paul K.
Title: Correlation analysis of pesticide use data and cancer incidence rates in California counties.
Published in: Archives of Environmental Health, volumn 53, pages 410-413, (1998).
Abstract:
"California, the leading agricultural state in the United States, has maintained a population-based cancer registry since 1988, and it also maintains a comprehensive, statewide pesticide reporting system. Data on cancer incidence and pesticide use reporting are available, by county, for all 58 counties in California. Average annual age-adjusted cancer incidence rates (1988-1992), on a county-, sex-, and race/ethnicity-specific basis, were obtained from the California Cancer Registry (CCR), which maintains the population-based cancer registry throughout California. Pesticide use data (i.e., pounds of active ingredient applied annually in each county) were obtained from the California Department of Pesticide Regulation for 1993. Investigators used Pearson product-moment correlation coefficients (r) to correlate age-adjusted incidence rates for selected cancers with the use data for selected pesticides.
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For most sex- and race/ethnicity-specific groups, the correlation coefficients were very close to zero or negative in sign, indicating no correlation between pesticide use and cancer incidence. There were, however, several exceptions, particularly in Hispanic males for whom the following correlations were observed: leukemia and atrazine (r = .40), leukemia and 2,4-dichlorophenoxyacetic acid (r = .41), leukemia and captan (r = .46), atrazine and brain cancer (r = .54), and atrazine and testicular cancer (r = .41). For black males, we observed the following: atrazine and prostate cancer (r = .67) and Captan and prostate cancer (r = .49). In females, only a few of the correlations were elevated. Although most of the correlations examined in this analysis were not elevated, several of those in the Hispanic and black male populations were. These segments of the population have traditionally been employed as farm workers in California and have had the greatest potential for exposure to pesticides. This was an ecological study for which no data about exposure to pesticides at the individual level were available for analysis. In addition, no latency period was allowed between potential exposure and diagnosis with cancer. However, the results obtained in two minority groups who represented the majority of farm workers in the fields suggested that additional research studies, in which more rigorous study designs are used, should be conducted in those groups."
Given the likelihood that those who were exposed to one pesticide or fungicide were also exposed to others, and perhaps had diets deficient in some things and overabundant in others, there is clearly a need for a more rigorous study design, one that will not label coincidence as a cause. A significant number of farm workers smoke, and the carcinogens in tobacco and its smoke very likely increase the numbers of cancers of various kinds, and perhaps act synergistically with other chemical agents to increase the incidence of various cancers. Is there any evidence that smokers were eliminated from the group studied? I’d hate to make major decisions based on these flawed data.
More than 50% of drug addicts and cancer patients have been exposed to milk in their lives. We do not say that milk by itself causes drug addiction or cancer–but perhaps it does increase the incidence under the right set of circumstances.
Peter, published research is subject to peer review. I assume that both the authors professional training and that of the reviewers are sufficient to prevent what you describe (the reviewers are normally chosen for their reputation in the field of the publication).
It would be nice to be able to assume those things, but since there is no mention of such things perhaps they should not be assumed–something like not assuming fragrance in a rose if the catalog doesn’t mention any. Recent scandals in scientific publications do not encourage the reader to accept reports without a healthy dose of skepticism.
Perhaps 20 years from now there will have been a definitive and useful study on this matter. Right now it seems that there has not been such a study and the rule is, as usual, let the buyer beware (and take sensible precautions).
The journal policies are given at the link below:
Also see:
Link: www.heldref.org/html/body_aeh_manu.html
Title: Captan. Documentation of proposed values of permissible occupational exposure levels.
Authors: Ludwicki, Jan K.; Strucinski, Pawel. Panstwowy Zaklad Higieny, Warsaw, Pol.
Journal: Podstawy i Metody Oceny Srodowiska Pracy, Volumn 17, pages 137-156 (2001)…
Abstract:
" 1,2,3,6-Tetrahydro-N-(trichloromethylthio)-phthalimide (captan) is a nonsystemic phthalimide fungicide used to control a wide range of fungal diseases of many fruit, ornamental, and vegetable (including potatoes) crops. In the available scientific literature there are no records on acute poisonings in human beings. There are also no data allowing estn. of the dose-effect relationship in occupationally exposed workers. Acute exposure to captan dust may cause an irritation of the eyes, skin, and upper respiratory tract, while chronic exposure is responsible for developing skin sensitization and dermatitis. The epidemiol. studies performed in 1988-1992 in California, USA, showed a weak correlation between exposure to captan and leukemia in Hispanic men and prostate cancer in black men. The rodent oral LD50 values for captan ranges from 7000 to 15,000 mg/kg b.w. (body wt.), indicating very low acute toxicity. Sheep and, to a lesser degree, cattle are much more susceptible to captan. The dermal LD50 for rabbit is >4500 mg/kg b.w. The inhalation LC50 (2 h) values for rodents are >4500 mg/m3.
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The results of 1- and 3-generation rat studies allowed establishment of a NOEL (no observable effect level) value (based on the decreased mean body wts. as an end-point) at the level of 12.5 mg/kg-day. Captan demonstrated the ability to induce gene mutations, usually in bacterial tests without metabolic activation, but most evidence indicates that it is not mutagenic in intact higher animals. Captan induced chromosomal aberrations, sister chromatid exchange, and mutations at several loci, but not unscheduled DNA synthesis, in cultured mammalian cells. Host-mediated assays and in vivo expts. have provided both pos. and neg. results. The carcinogenic potential of the fungicide has been evidenced in one strain of mice, inducing duodenal tumors. No evidence of carcinogenicity was found in numerous other studies.
Captan has shown little, if any, embryotoxic or teratogenic potential in mice or rats at maternally tolerated doses. The results obtained in tests with other species were considered inconclusive. The wt. of evidence suggests that captan does not produce birth defects. Captan is readily absorbed from the gastrointestinal tract as well as by inhalation. It is rapidly metabolized and excreted primarily in the urine. One of biotransformation pathways of captan leads to formation of chem. active thiophosgene. The proposed max. exposure limit (MAC), 5 mg/m3, is based on the NOEL value (12.5 mg/kg b.w.-day) derived from long-term (1- and 3-generation) feeding studies on rats. It is in accordance with MAC values binding in other European countries (including the EU) and in the USA."