Multiple pesticide exposures and the risk of multiple myeloma in Canadian men

Abstract

Multiple myeloma (MM) has been linked to certain agricultural exposures, including pesticides. This analysis aimed to investigate the association between lifetime use of multiple pesticides and MM risk using two exposure metrics: number of pesticides used and days per year of pesticide use. A frequency-matched, population-based case-control study was conducted among men in six Canadian provinces between 1991 and 1994. Data from 342 MM cases and 1,357 controls were analyzed using logistic regression to calculate odds ratios (OR) and 95% confidence intervals. Pesticides were grouped by type, chemical class and carcinogenic potential, using a composite carcinogenic probability score. Selected individual pesticides were also examined. Regression models were adjusted for age, province of residence, use of proxy respondents, smoking and selected medical history variables. The overall pattern of results was complex. Positive trends in risk were observed for fungicides (p trend 50.04) and pesticides classified as probably carcinogenic or higher (p trend 50.03). Excess risks of MM were observed among men who reported using at least one carbamate pesticide (OR51.94, 1.16-3.25), one phenoxy herbicide (OR51.56, 1.09-2.25) and 3 organochlorines (OR52.21, 1.05-4.66). Significantly higher odds of MM were seen for exposure to carbaryl (OR52.71, 1.47-5.00) and captan (OR52.96, 1.40-6.24). Use of mecoprop for >2 days per year was also significantly associated with MM (OR52.15, 1.03-4.48). Focusing on multiple pesticide exposures is important because this more accurately reflects how exposures occur in occupational settings. Significant associations observed for certain chemical classes and individual pesticides suggest that these may be MM risk factors.

Glyphosate epidemiology expert panel review: a weight of evidence systematic review of the relationship between glyphosate exposure and non-Hodgkin’s lymphoma or multiple myeloma

“…Analyses of next-of-kin or proxy respondents have been found to produce results similar to those of first-hand study subjects (e.g. Kachuri et al 2013) or to show results quite different than those based on first-hand responders (e.g. Lee et al 2005 -ORs for glyphosate and glioma were 0.4 based on primary respondents and 3.1 for proxy respondents); one never knows the impact of having appreciable numbers of next-of-kin respondents without a thorough analysis of data with/without proxy respondents (Johnson et al 1993).…”

“…The publication is related to the trans-Canada NHL study reported initially by McDuffie et al (2001) wherein there was a common control group for the study of several lymphopoietic cancers. Pahwa et al (2012) was updated by Kachuri et al (2013) and we defer consideration to that more recent publication. Kachuri et al (2013) presented a reanalysis and extension of Pahwa et al (2012) in which they excluded 149 (of 1506) controls who did not have an age match with the MM cases.…”

“…Pahwa et al (2012) was updated by Kachuri et al (2013) and we defer consideration to that more recent publication. Kachuri et al (2013) presented a reanalysis and extension of Pahwa et al (2012) in which they excluded 149 (of 1506) controls who did not have an age match with the MM cases. Kachuri et al utilized unconditional logistic regression to estimate ORs and presented analyses including and excluding proxy respondents (15% of controls and 30% of cases) and adjusting for smoking, which was associated with MM.…”

Human Health Risks of the Use of Glyphosate and Glyphosate-Based Herbicides: Review

“…80 Kanada'da yaşam süresi boyunca pestisit maruziyeti ve multipl miyelom ilişkisi araştırılmış, glifosata kısa zamanlı (≤2 gün/yıl) maruz kalan bireylerde herhangi bir ilişki bulunmaz iken (OR: 0,72, %95 CI, 0,39-1,32), uzun süre (>2 gün/yıl) maruz kalan bireylerde ilişki bulunmuştur (OR: 2,04, %95 CI, 0,98-4,23). 81 …”

Understanding the multiple biological aspects leading to myeloma

“…7,15 Environmental risk factors have also been implicated in increasing MM risk, including obesity, 16,17 immune dysfunction (including auto-immune disease, HIV and transplantation), [18][19][20] and agricultural or industrial exposure to chemicals, pesticides or radiation. 21,22 A key hypothesis that has been addressed in numerous studies is that genetic variation governing individual response to environmental exposures may mediate some of the familial aggregation seen in MM. The descriptions of families with more than one case of MM support the suggestion that there is an underlying genetic predisposition with an increased relative risk of developing MM for first degree relatives (increased risk of developing MM (RR=2.1; 95%CI: 1.6-2.9) and of developing MGUS (RR=2.1; 95%CI: 1.5-3.1)).…”