Asthma history, occupational exposure to pesticides and the risk of non‐Hodgkin's lymphoma

Lee, Won Jin; Purdue, Mark P.; Stewart, Patricia A.; Schenk, Mary Jean; Roos, Anneclaire J. De; Cerhan, James R.; Severson, Richard K.; Cozen, Wendy; Hartge, Patricia; Blair, Aaron

doi:10.1002/ijc.21755

Cited by 5 publications

(17 citation statements)

References 15 publications

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“…Furthermore, this study17 found an identical risk of NHL from DDT exposure for non‐asthmatic farmers (OR = 1.2, 95% CI: 0.9–1.5) and asthmatic farmers (OR = 1.2, 95% CI: 0.6–2.4), whereas our analysis showed a higher risk of NHL among asthmatics who used DDT. Another study from Iowa, Los Angeles County, Seattle, and the Detroit Metropolitan Area18 found that the odds of NHL associated with probable occupational exposure to pesticides was higher among asthmatics (OR = 1.7, 95% CI: 0.3–9.1) compared to non‐asthmatics (OR = 0.9, 95% CI: 0.6–1.5), which is what we observed for overall pesticide use. Vajdic et al ,19 in an evaluation of the effects of asthma, hay fever, eczema, and food allergy on the association between pesticide exposure and risk of NHL, observed that the odds of NHL with substantial pesticide exposure and any history of asthma was 3.07 (95% CI: 0.55–17.10); while for no asthma history, the risk was 4.23 (95% CI: 1.76–10.16).…”

Section: Discussionsupporting

confidence: 77%

“…We also evaluated the effects of a group comprised of other immune conditions (hay fever, celiac disease, rheumatoid arthritis, or acne) in an exploratory fashion. These conditions were selected for analysis because they had been hypothesized to increase NHL risk,7 were available in the CCSPH, and were relevant to earlier studies that explored the potential effect modification of asthma,17–19 hay fever, eczema, and food allergy19 on pesticide exposure and NHL risk. NHL risks were estimated from these groups of immunologic conditions and self‐reported ever/never use of: ( i ) any pesticide; ( ii ) any organochlorine insecticide; ( iii ) any organophosphate insecticide; ( iv ) any phenoxy herbicide; ( v ) selected individual pesticides [1,1′‐(2,2,2‐trichloroethylidene)bis[4‐chlorobenzene]; 1,1,1‐trichloro‐2,2‐bis(4‐chlorophenyl) ethane (DDT), malathion, (4‐chloro‐2‐methylphenoxy)acetic acid (MCPA), mecoprop, and (2,4‐dichlorophenoxy)acetic acid (2,4‐D)]; and ( vi ) from the number of potentially carcinogenic pesticides reportedly used (see Appendix A for a complete list of pesticides in these six groups).…”

Section: Methodsmentioning

confidence: 99%

“…Multiple logistic regression was used to calculate crude and adjusted odds ratios (ORs) and 95% confidence intervals (CIs) between the six pesticide use groups defined earlier and the risk of NHL using SAS software (SAS Institute, Cary, NC, Version 9.1). ORs were adjusted for age, province of residence, respondent type (self or proxy), and diesel oil exposure, which were found to be relevant confounders in the literature 14, 17–19, 24. A stratified analysis based on the a priori immunologic categories was conducted to estimate adjusted ORs for the association between pesticide use and risk of NHL.…”

Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

“…Studies of the effect of immune conditions on pesticide exposure and NHL risk have generated inconsistent results 17–19. Two population‐based case–control investigations in the United States found that the relative risk of NHL from pesticide exposure was elevated among asthmatics compared to non‐asthmatics 17–18. Conversely, an Australian population‐based case–control study found no effect of asthma and other immunologic conditions on the relationship between pesticide exposure and NHL risk 19.…”

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confidence: 99%

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Modulation of the angiogenic phenotype of normal and systemic sclerosis endothelial cells by gain–loss of function of pentraxin 3 and matrix metalloproteinase 12

Margheri¹,

Serratì²,

Lapucci³

et al. 2010

Arthritis & Rheumatism

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Objective. Studies have shown that in systemic sclerosis (SSc) endothelial cells, overproduction of matrix metalloproteinase 12 (MMP-12) and pentraxin 3 (PTX3) is associated with defective angiogenesis. This study was undertaken to examine whether overexpression of the relevant molecules could inhibit angiogenesis of normal microvascular endothelial cells (MVECs), and whether silencing of these molecules in SSc MVECs could restore the lost angiogenic properties of the cells in vitro and in vivo.Methods. Transient transfection of MVECs with human MMP12 and PTX3 was performed by electroporation. Silencing of MMP12 and PTX3 was obtained by treatment with small interfering RNA, and treatment effects were validated by Western blotting with specific antibodies and a fluorimetric assay. In vitro cell migration and capillary morphogenesis were studied on Matrigel substrates. In vivo angiogenesis was studied using a Matrigel sponge assay in mice.Results Many human diseases that involve alterations of the angiogenic process, including cancer and inflammatory conditions, are characterized by excess angiogenesis (1-4). In contrast, in systemic sclerosis (SSc), the pathologic abnormalities affecting microvessels and the breakdown of their patency leads to chronic tissue hypoxia and to capillary loss, which in turn leads to vital organ failure (5). These features suggest that there is an insufficient angiogenic response occurring in SSc (6), despite the tissue hypoxia that characterizes the disease.

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Section: Discussionsupporting

confidence: 77%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Modulation of the angiogenic phenotype of normal and systemic sclerosis endothelial cells by gain–loss of function of pentraxin 3 and matrix metalloproteinase 12

Margheri¹,

Serratì²,

Lapucci³

et al. 2010

Arthritis & Rheumatism

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Atopy, exposure to pesticides and risk of non‐Hodgkin lymphoma

Vajdic

Fritschi

Grulich

et al. 2007

Intl Journal of Cancer

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Pesticide exposure has been associated with non-Hodgkin lymphoma (NHL) risk in a number of studies, and two recent studies suggest that the increased risk may be confined to those with a history of asthma. We examined the interaction between occupational pesticide exposure and atopy on risk of NHL in an Australian population-based case-control study. Incident cases (n 5 694) were diagnosed in New South Wales or the Australian Capital Territory between 2000 and 2001 and controls (n 5 694) were randomly selected from electoral rolls and frequency-matched to cases by age, sex and State of residence. Occupational pesticide exposure was determined by an expert occupational hygienist's assessment of job-specific questionnaires administered by telephone. History of atopy (asthma, hay fever, eczema and food allergy) was self-reported. Logistic regression models included the three matching variables, ethnicity and sun exposure. The OR for NHL with substantial pesticide exposure and any history of asthma was 3.07 (95% CI 0.55-17.10) and with substantial pesticide exposure and no asthma history it was 4.23 (95% CI 1.76-10.16). The p-value for interaction was 0.29. A similar pattern of risk was observed for each of the pesticide subtypes; for asthma at various times of life; for hay fever, eczema, food allergy and any atopy, in men only and for follicular lymphomas only. Although this study had limited power, the findings do not suggest modification of the association between pesticide exposure and NHL risk by asthma or atopic disease more generally. ' 2007 Wiley-Liss, Inc.Key words: non-Hodgkin lymphoma; risk; case-control; pesticides; asthma; atopy Occupational exposure to pesticides and a personal history of atopy have been widely examined as risk factors for non-Hodgkin lymphoma (NHL), a neoplasm arising from cells of the immune system. These studies have typically found that exposure to pesticides increases risk of NHL, 1 while asthma, or atopy more generally, has been inconsistently protective.2 Since both pesticide exposure and asthma may influence NHL risk by modulating the immune system, 2 US studies of NHL examined the interaction between the 2 exposures; they found that risk of NHL with pesticide exposure was higher in asthmatics than in non-asthmatics. 3,4 Although there is no biological evidence that asthma modifies the effect of pesticide exposure on NHL risk, given the potential importance of such a relationship, we sought to replicate it in our case-control study of NHL in Australia. We have previously reported an odds ratio of 3.09 (95% CI 1.42-6.70) for NHL with substantial occupational pesticide exposure 5 and apparently protective effects of having asthma (OR 0.88, 95% CI 0.67-1.17), eczema (OR 0.72, 95% CI 0.57-1.10) or hay fever (OR 0.65, 95% CI 0.52-0.82) as an adult, or for being allergic to one or more foods at any time of life (OR 0.29, 95% CI 0.20-0.42). 6 Material and methodsDetailed methods for this study have been described previously. [5][6][7]

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Pesticide use, immunologic conditions, and risk of non‐Hodgkin lymphoma in Canadian men in six provinces

Pahwa

Harris

Hohenadel

et al. 2012

Intl Journal of Cancer

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Pesticide exposures and immune suppression have been independently associated with the risk of non-Hodgkin lymphoma (NHL), but their joint effect has not been well explored. Data from a case-control study of men from six Canadian provinces were used to evaluate the potential effect modification of asthma, allergies, or asthma and allergies and hay fever combined on NHL risk from use of: (i) any pesticide; (ii) any organochlorine insecticide; (iii) any organophosphate insecticide; (iv) any phenoxy herbicide; (v) selected individual pesticides [1,1'-(2,2,2-trichloroethylidene)bis [4-chlorobenzene]; 1,1,1-trichloro-2,2-bis(4-chlorophenyl) ethane (DDT), malathion, (4-chloro-2-methylphenoxy)acetic acid (MCPA), mecoprop, and (2,4-dichlorophenoxy)acetic acid (2,4-D); and (vi) from the number of potentially carcinogenic pesticides. Incident NHL cases (n 5 513) diagnosed between 1991 and 1994 were recruited from provincial cancer registries and hospitalization records and compared to 1,506 controls. A stratified analysis was conducted to calculate odds ratios (ORs) adjusted for age, province, proxy respondent, and diesel oil exposure. Subjects with asthma, allergies, or hay fever had non-significantly elevated risks of NHL associated with use of MCPA (OR 5 2.67, 95% confidence interval [CI]: 0.90-7.93) compared to subjects without any of these conditions (OR 5 0.81, 95% CI: 0.39-1.70). Conversely, those with asthma, allergies, or hay fever who reported use of malathion had lower risks of NHL (OR 5 1.25, 95% CI: 0.69-2.26) versus subjects with none of these conditions (OR 5 2.44, 95% CI: 1.65-3.61). Similar effects were observed for asthma and allergies evaluated individually. Although there were some leads regarding effect modification by these immunologic conditions on the association between pesticide use and NHL, small numbers, measurement error and possible recall bias limit interpretation of these results.The incidence of non-Hodgkin lymphoma (NHL) showed a steady worldwide increase from 1950, but plateaued in the late 1990s.1 In 2011, NHL was the fifth most frequently occurring cancer and the sixth leading cause of all cancer deaths in Canada.2 The causes of NHL are not well-known. 1,3Immune suppression is the most clearly established risk factor for NHL 3-6 because of substantially elevated risks among individuals with autoimmune disease, primary or acquired immunodeficiencies, and organ transplant recipients.1,3 Risk appears to increase with the degree of immune deficiency.7 Factors that suppress the immune system, like chemical exposures, may facilitate the development of NHL. A number of occupational and environmental factors have been associated with NHL. 5,8 Farming has been linked to NHL 9 overall and for major NHL subtypes. 1 This observation has prompted research on agricultural chemicals, such as pesticides, solvents, fuels, oils, and other agents that are potentially carcinogenic. [10][11][12] Use of some specific pesticides may contribute to the increased incidence of NHL.13-15 For example, occupationa...

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Asthma history, occupational exposure to pesticides and the risk of non‐Hodgkin's lymphoma

Cited by 5 publications

References 15 publications

Modulation of the angiogenic phenotype of normal and systemic sclerosis endothelial cells by gain–loss of function of pentraxin 3 and matrix metalloproteinase 12

Modulation of the angiogenic phenotype of normal and systemic sclerosis endothelial cells by gain–loss of function of pentraxin 3 and matrix metalloproteinase 12

Atopy, exposure to pesticides and risk of non‐Hodgkin lymphoma

Pesticide use, immunologic conditions, and risk of non‐Hodgkin lymphoma in Canadian men in six provinces

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