Bibliography Tag: epidemiological studies

Bibliography Index

Cocco et al., 2013

Cocco, Pierluigi, Satta, Giannina, Dubois, Stefania, Pili, Claudia, Pilleri, Michela, Zucca, Mariagrazia, ‘t Mannetje, Andrea Martine, Becker, Nikolaus, Benavente, Yolanda, de Sanjosé, Silvia, Foretova, Lenka, Staines, Anthony, Maynadié, Marc, Nieters, Alexandra, Brennan, Paul, Miligi, Lucia, Ennas, Maria Grazia, & Boffetta, Paolo, “Lymphoma risk and occupational exposure to pesticides: results of the EPILYMPH study,” Occupational and Environmental Medicine, 2013, 70(2), 91, DOI: 10.1136/oemed-2012-100845.

ABSTRACT:

OBJECTIVES: We investigated the role of occupational exposure to specific groups of agrochemicals in the aetiology of lymphoma overall, B cell lymphoma and its most prevalent subtypes.

METHODS: In 1998–2003, 2348 incident lymphoma cases and 2462 controls were recruited to the EPILYMPH case-control study in six European countries. A detailed occupational history was collected in cases and controls. Job modules were applied for farm work including specific questions on type of crop, farm size, pests being treated, type and schedule of pesticide use. In each study centre, industrial hygienists and occupational experts assessed exposure to specific groups of pesticides and individual compounds with the aid of agronomists. We calculated the OR and its 95% CI associated with lymphoma and the most prevalent lymphoma subtypes with unconditional logistic regression, adjusting for age, gender, education and centre.

RESULTS: Risk of lymphoma overall, and B cell lymphoma was not elevated, and risk of chronic lymphocytic leukaemia (CLL) was elevated amongst those ever exposed to inorganic (OR=1.6, 95% CI 1.0 to 2.5) and organic pesticides (OR=1.5, 95% CI 1.0 to 2.1). CLL risk was highest amongst those ever exposed to organophosphates (OR=2.7, 95% CI 1.2 to 6.0). Restricting the analysis to subjects most likely exposed, no association was observed between pesticide use and risk of B cell lymphoma.

CONCLUSIONS: Our results provide limited support to the hypothesis of an increase in risk of specific lymphoma subtypes associated with exposure to pesticides. FULL TEXT

Hohenadel et al., 2011

Hohenadel, Karin, Harris, Shelley A, McLaughlin, John R, Spinelli, John J, Pahwa, Punam, Dosman, James A, Demers, Paul A, & Blair, Aaron., “Exposure to multiple pesticides and risk of non-Hodgkin lymphoma in men from six Canadian provinces,” International Journal of Environmental Research and Public Health, 2011, 8(6), 2320-2330. doi:10.3390/ijerph8062320.

ABSTRACT:

Non-Hodgkin lymphoma (NHL) has been linked to several agricultural exposures, including some commonly used pesticides. Although there is a significant body of literature examining the effects of exposure to individual pesticides on NHL, the impact of exposure to multiple pesticides or specific pesticide combinations has not been explored in depth. Data from a six-province Canadian case-control study conducted between 1991 and 1994 were analyzed to investigate the relationship between NHL, the total number of pesticides used and some common pesticide combinations. Cases (n=513) were identified through hospital records and provincial cancer registries and controls (n=1,506), frequency matched to cases by age and province of residence, were obtained through provincial health records, telephone listings, or voter lists. In multiple logistic regression analyses, risk of NHL increased with the number of pesticides used. Similar results were obtained in analyses restricted to herbicides, insecticides and several pesticide classes. Odds ratios increased further when only ‘potentially carcinogenic’ pesticides were considered (OR[one pesticide]=1.30, 95% CI=0.90-1.88; OR[two to four]=1.54, CI=1.11-2.12; OR[five or more]=1.94, CI=1.17-3.23). Elevated risks were also found among those reporting use of malathion in combination with several other pesticides. These analyses support and extend previous findings that the risk of NHL increases with the number of pesticides used and some pesticide combinations. FULL TEXT

Harari et al., 2010

Harari, Raul, Julvez, Jordi, Murata, Katsuyuki, Barr, Dana, Bellinger, David C., Debes, Frodi, & Grandjean, Philippe, “Neurobehavioral deficits and increased blood pressure in school-age children prenatally exposed to pesticides,” Environmental Health Perspectives, 118, 890-896, 2010, doi:10.1289/ehp.0901582.

ABSTRACT:

BACKGROUND: The long-term neurotoxicity risks caused by prenatal exposures to pesticides are unclear, but a previous pilot study of Ecuadorian school children suggested that blood pressure and visuospatial processing may be vulnerable.

OBJECTIVES: In northern Ecuador, where floriculture is intensive and relies on female employment, we carried out an intensive cross-sectional study to assess children’s neurobehavioral functions at 6-8 years of age.

METHODS: We examined all 87 children attending two grades in the local public school with an expanded battery of neurobehavioral tests. Information on pesticide exposure during the index pregnancy was obtained from maternal interview. The children’s current pesticide exposure was assessed from the urinary excretion of organophosphate metabolites and erythrocyte acetylcholine esterase activity.

RESULTS: Of 84 eligible participants, 35 were exposed to pesticides during pregnancy via maternal occupational exposure, and 23 had indirect exposure from paternal work. Twenty-two children had detectable current exposure irrespective of their prenatal exposure status. Only children with pre-natal exposure from maternal greenhouse work showed consistent deficits after covariate adjustment, which included stunting and socioeconomic variables. Exposure-related deficits were the strongest for motor speed (Finger Tapping Task), motor coordination (Santa Ana Form Board), visuospatial performance (Stanford-Binet Copying Test), and visual memory (Stanford-Binet Copying Recall Test). These associations corresponded to a developmental delay of 1.5-2 years. Prenatal pesticide exposure was also significantly associated with an average increase of 3.6 mmHg in systolic blood pressure and a slight decrease in body mass index of 1.1 kg/m2. Inclusion of the pilot data strengthened these results.

CONCLUSIONS: These findings support the notion that prenatal exposure to pesticides-at levels not producing adverse health outcomes in the mother-can cause lasting adverse effects on brain development in children. Pesticide exposure therefore may contribute to a “silent pandemic” of developmental neurotoxicity. FULL TEXT

McDuffie et al., 2001

Helen H. McDuffie, Punam Pahwa, John R. McLaughlin, John J. Spinelli, Shirley Fincham, James A. Dosman, Diane Robson, Leo F. Skinnider and Norman W. Choi, “Non-Hodgkin’s Lymphoma and Specific Pesticide Exposures in Men: Cross-Canada Study of Pesticides and Health,” Cancer Epidemiology, Biomarkers, & Prevention, 2001, 10.

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 variables (history of measles, mumps, cancer, allergy desensitization treatment, and a positive history of cancer in first-degree relatives). 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. 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. FULL TEXT

Rull et al., 2006

Rudolph P. Rull Beate Ritz Gary M. Shaw, “Neural Tube Defects and Maternal Residential Proximity to Agricultural Pesticide Applications,” American Journal of Epidemiology, 163:8, 15 April 2006, DOI: 10.1093/aje/kwj101

ABSTRACT:

Residential proximity to applications of agricultural pesticides may be an important source of exposure to agents that have been classified as developmental toxins. Data on two case-control study populations of infants with neural tube defects (NTDs) and nonmalformed controls delivered in California between 1987 and 1991 were pooled to investigate whether maternal residential proximity to applications of specific pesticides or physicochemical groups of pesticides during early gestation increases the risk of these malformations. Maternal residential proximity within 1,000 m of pesticide applications was ascertained by linking mothers’ addresses with agricultural pesticide use reports and crop maps. Odds ratios were computed by using conventional single- and multiplepesticide and hierarchical multiple-pesticide logistic regression. In single-pesticide models, several pesticides were associated with NTDs after adjustment for study population, maternal ethnicity, educational level, cigarette smoking, and vitamin use. In a hierarchical multiple-pesticide model, effect estimates for only benomyl and methomyl suggested a possible association. Elevated risks of NTDs and anencephaly or spina bifida subtypes were also  associated with exposures to chemicals classified as amide, benzimidazole, methyl carbamate, or organophosphorus pesticides and with increasing numbers of pesticides. These results suggest that ambient exposure to certain categories of agricultural pesticides may increase the risk of NTDs.  FULL TEXT

Benbrook, 2016c

John Peterson Myers, Michael N. Antoniou, Bruce Blumberg, Lynn Carroll, Theo Colborn, Lorne G. Everett, Michael Hansen, Philip J. Landrigan, Bruce P. Lanphear, Robin Mesnage, Laura N. Vandenberg, Frederick S. vom Saal, Wade V. Welshons and Charles M. Benbrook. “Concerns over use of glyphosate-based herbicides and risks associated with exposures: a consensus statement,” Environmental Health, 2016, 15:19, DOI: 10.1186/s12940-016-0117-0.

ABSTRACT:

The broad-spectrum herbicide glyphosate (common trade name “Roundup”) was first sold to farmers in 1974. Since the late 1970s, the volume of glyphosate-based herbicides (GBHs) applied has increased approximately 100-fold. Further increases in the volume applied are likely due to more and higher rates of application in response to the widespread emergence of glyphosate-resistant weeds and new, pre-harvest, dessicant use patterns. GBHs were developed to replace or reduce reliance on herbicides causing well-documented problems associated with drift and crop damage, slipping efficacy, and human health risks. Initial industry toxicity testing suggested that GBHs posed relatively low risks to non-target species, including mammals, leading regulatory authorities worldwide to set high acceptable exposure limits. To accommodate changes in GBH use patterns associated with genetically engineered, herbicide-tolerant crops, regulators have dramatically increased tolerance levels in maize, oilseed (soybeans and canola), and alfalfa crops and related livestock feeds. Animal and epidemiology studies published in the last decade, however, point to the need for a fresh look at glyphosate toxicity. Furthermore, the World Health Organization’s International Agency for Research on Cancer recently concluded that glyphosate is “probably carcinogenic to humans.” In response to changing GBH use patterns and advances in scientific understanding of their potential hazards, we have produced a Statement of Concern drawing on emerging science relevant to the safety of GBHs. Our Statement of Concern considers current published literature describing GBH uses, mechanisms of action, toxicity in laboratory animals, and epidemiological studies. It also examines the derivation of current human safety standards. We conclude that: (1) GBHs are the most heavily applied herbicide in the world and usage continues to rise; (2) Worldwide, GBHs often contaminate drinking water sources, precipitation, and air, especially in agricultural regions; (3) The half-life of glyphosate in water and soil is longer than previously recognized; (4) Glyphosate and its metabolites are widely present in the global soybean supply; (5) Human exposures to GBHs are rising; (6) Glyphosate is now authoritatively classified as a probable human carcinogen; (7) Regulatory estimates of tolerable daily intakes for glyphosate in the United States and European Union are based on outdated science. We offer a series of recommendations related to the need for new investments in epidemiological studies, biomonitoring, and toxicology studies that draw on the principles of endocrinology to determine whether the effects of GBHs are due to endocrine disrupting activities. We suggest that common commercial formulations of GBHs should be prioritized for inclusion in government-led toxicology testing programs such as the U.S. National Toxicology Program, as well as for biomonitoring as conducted by the U.S. Centers for Disease Control and Prevention.  FULL TEXT

Perry et al., 2006

Melissa J. Perry, Anne Marbella, Peter M. Layde, “Nonpersistent Pesticide Exposure Self-report versus Biomonitoring in Farm Pesticide Applicators,” Annals of Epidemiology, 2006, 16:9, DOI: 10.1016/J.ANNEPIDEM.2005.12.004.

ABSTRACT:

PURPOSE: Few studies using biologic markers to examine nonpersistent pesticide exposure among pesticide applicators were conducted in field settings. This study compares self-reported dermal, inhalation, and ingestion exposures with urinalysis results after one-time application of the commonly used herbicide atrazine to field crops. It was hypothesized that: i) applicator reports of exposure would be associated positively with detection of urinary atrazine metabolites, and ii) applicator reports of personal-protective-equipment (PPE) use would be associated negatively with detection of urinary atrazine metabolites.

METHODS: Wisconsin dairy farmers were randomly selected to participate in 1997 to 1998 and were instructed to collect a urine sample 8 hours after the first pesticide application of the season. Farmers then were interviewed within 1 week of their first application to report on application practices. Eighty-six urine samples were analyzed for deethylatrazine, a major atrazine metabolite.

RESULTS: Comparing urinalysis results with self-reported dermal, inhalation, and ingestion exposure showed poor agreement between self-reported exposure and urinary deethylatrazine detections (all κ < 0.40). Multivariate linear regression modeling with deethylatrazine level as the outcome showed that self-reported practices did not significantly predict atrazine metabolite levels.

CONCLUSIONS: Possible explanations for the discrepancies between urinalysis results and self-reported data include: i) inaccuracies in self-reported data and ii) substantial interpersonal variation in atrazine metabolism, resulting in major differences in body burden for similar exposures. Either explanation poses challenges for epidemiologic studies of the health effects of pesticides, which rely solely on self-reported measures of exposure. Additional evaluation of determinants of accuracy in self-assessed occupational and environmental exposures is needed.

Winchester et al., 2009

Winchester PD, Huskins J, Ying J, “Agrichemicals in surface water and birth defects in the United States,” Acta Paediatrica, 2009, 98:4, DOI: 10.1111/j.1651-2227.2008.01207.

ABSTRACT:

OBJECTIVES: To investigate if live births conceived in months when surface water agrichemicals are highest are at greater risk for birth defects.

METHODS: Monthly concentrations during 1996-2002 of nitrates, atrazine and other pesticides were calculated using United States Geological Survey’s National Water Quality Assessment data. Monthly United States birth defect rates were calculated for live births from 1996 to 2002 using United States Centers for Disease Control and Prevention natality data sets. Birth defect rates by month of last menstrual period (LMP) were then compared to pesticide/nitrate means using logistical regression models.

RESULTS: Mean concentrations of agrichemicals were highest in April-July. Total birth defects, and eleven of 22 birth defect subcategories, were more likely to occur in live births with LMPs between April and July. A significant association was found between the season of elevated agrichemicals and birth defects.

CONCLUSION: Elevated concentrations of agrichemicals in surface water in April-July coincided with higher risk of birth defects in live births with LMPs April-July. While a causal link between agrichemicals and birth defects cannot be proven from this study an association might provide clues to common factors shared by both variables.    FULL TEXT

Winchester et al., 2016

Winchester P, Proctor C, Ying J, “County-level pesticide use and risk of shortened gestation and preterm birth,” Acta Paediatrica, 2016, 105:3, DOI: 10.1111/apa.13288.

ABSTRACT:

AIM: This study assesses the association between pesticide exposure in pregnancy, preterm birth (PTB) and shortened gestation.

METHODS: Pregnancy information was abstracted from the Centers for Disease Control (CDC) Non-Public Use Natality Datasets 1990-2005. Pesticide use in maternal county of residence was calculated using California Pesticide Use Reporting (PUR) data 1990-2005. Counties were ranked by pesticide use, and birth months were sorted by peak (May-June) or nonpeak (other months) pesticide use. Multivariate logistical regression models were used.

RESULTS: Counties with higher pesticide use were associated with higher PTB (low 8.59 ± 0.11%, moderate 9.25 ± 0.07%, high 10.0 ± 0.06%, p’s < 0.001) and shorter gestations (low 39.197 ± 0.014 weeks, moderate 39.126 ± 0.011 weeks, high 39.049 ± 0.011 weeks, p’s < 0.001). Peak pesticide months were associated with higher PTB (10.01 ± 0.05% vs. 9.36 ± 0.05%, p < 0.001) and shorter gestations (39.069 ± 0.007 weeks vs. 39.122 ± 0.007 weeks, p < 0.001). The pesticide effect on shortened gestation and higher PTB was found in all racial groups. Pesticide use was highest for fungicides > insecticides > fumigants > herbicides > others. Each pesticide type was found to be associated with higher PTB and shorter gestation.

CONCLUSION: PTB and shortened gestation were significantly associated with pesticide use in maternal county of residence regardless of race, gestation at birth, and in most risk categories.   FULL TEXT

Rocheleau et al., 2009

Rocheleau CM, Romitti PA, Dennis LK, “Pesticides and hypospadias: a meta-analysis.,” Journal of Pediatric Urology, 2009, 5:1, DOI: 10.1016/j.jpurol.2008.08.006.

ABSTRACT:

OBJECTIVE: To use meta-analytic techniques to synthesize the findings of the current body of published literature regarding the risk of hypospadias resulting from parental exposure to pesticides.

MATERIALS AND METHODS: A search of Pub Med for original research published in English from January 1966 through March 2008 identified 552 studies, 90 of which were reviewed in detail. Nine studies met all study inclusion criteria. Two reviewers independently abstracted data from each included study. Any disagreements were resolved by consensus. Pooled risk ratios (PRRs) and confidence intervals (CIs) were calculated using both random and fixed effects models, along with statistical tests of homogeneity.

RESULTS: Elevated but marginally significant risks of hypospadias were associated with maternal occupational exposure (PRR of 1.36, CI=1.04-1.77), and paternal occupational exposure (PRR of 1.19, CI=1.00-1.41). Subgroup analyses provided insights into needed designs for future studies. Notably, exposure assessment using a job-exposure matrix resulted in slightly higher estimated risk than agricultural occupation in fathers; but this effect was reversed in mothers, suggesting the importance of indirect and residential pesticide exposures in this group.

CONCLUSIONS: Despite potential exposure misclassification, which would tend to diminish observed associations, the previous literature indicates a modestly increased risk of hypospadias associated with pesticide exposure.   FULL TEXT

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