A case-control study on cigarette,alcohol, and coffee consumption preceding Parkinson's disease

OBJECTIVE: To investigate the association between cigarette smoking, alcohol drinking, coffee consumption and Parkinson's disease (PD). METHODS: We selected subjects affected by idiopathic PD, with a Mini-Mental State Examination of > or =24, and controls matched 1 to 1 with cases by age (+/- 2 years) and sex. Controls were randomly selected from the resident list of the same municipality of residence of the cases. We assessed cigarette smoking, alcohol drinking, and coffee consumption preceding the onset of PD or the corresponding time for controls using a structured questionnaire, which also evaluated the duration and dose of exposure. Using conditional logistic regression analysis, we calculated adjusted OR and 95% CI. RESULTS: We interviewed 150 PD patients and 150 matched controls. Cigarette smoking (ever vs. never smokers OR = 0.66, 95% CI = 0.41-1.05, p = 0.08) did not show a statistically significant association with PD. We observed an inverse association between alcohol drinking (ever vs. never OR = 0.61, 95% CI = 0.39-0.97, p = 0.037) and coffee consumption (ever vs. never OR = 0.16, 95% CI 0.05-0.46, p = 0.0001) and PD. These associations remained significant after adjustment for other covariates: OR for ever vs. never alcohol consumption was 0.62 (95% CI = 0.43-0.89, p = 0.009) and that for coffee drinking 0.19 (95% CI = 0.07-0.52, p = 0.001). Heavy coffee consumption confirmed the inverse association between coffee and PD (more than 81 cup/year vs. none: OR = 0.20, 95% CI = 0.08-0.47, p < or = 0.0001). CONCLUSIONS: Consistent with previous studies, our results suggest an inverse association between coffee drinking, alcohol consumption and PD. The multiple inverse association observed may indicate a complex interaction between genetic and environmental factors.     

Smoking, alcohol, and coffee consumption preceding Parkinson's disease: a case-control study

OBJECTIVE: To study the association of PD with preceding smoking, alcohol, and coffee consumption using a case-control design. METHODS: The authors used the medical records linkage system of the Rochester Epidemiology Project to identify 196 subjects who developed PD in Olmsted County, MN, during the years 1976 to 1995. Each incident case was matched by age (+/-1 year) and sex to a general population control subject. The authors reviewed the complete medical records of cases and control subjects to abstract exposure information. RESULTS: For coffee consumption, the authors found an OR of 0.35 (95% CI = 0.16 to 0.78, p = 0.01), a dose-effect trend (p = 0.003), and a later age at PD onset in cases who drank coffee compared with those who never did (median 72 versus 64 years; p = 0.0002). The inverse association with coffee remained significant after adjustment for education, smoking, and alcohol drinking and was restricted to PD cases with onset at age <72 years and to men. The OR for cigarette smoking was 0.69 (95% CI = 0.45 to 1.08, p = 0.1). The authors found no association between PD and alcohol consumption. Extreme or unusual behaviors such as tobacco chewing or snuff use and a diagnosis of alcoholism were significantly more common in control subjects than cases. CONCLUSIONS: These findings suggest an inverse association between coffee drinking and PD; however, this association does not imply that coffee has a direct protective effect against PD. Alternative explanations for the association should be considered.     

Familial and environmental risk factors in Parkinson's disease: a case-control study in north-east Italy

BACKGROUND AND OBJECTIVE: The aetiology of Parkinson's disease remains unknown, although both genetic susceptibility and environmental factors are considered putative contributors to its origin. We performed a case-control study to investigate the association of familial and environmental risk factors with Parkinson's disease (PD). METHODS: We studied 136 patients with neurologist confirmed PD and 272 age- and sex-matched controls, affected by neurological diseases not related to PD. The risk of developing idiopathic PD associated with the following familial and environmental factors: positive family history of PD, positive family history of essential tremor (ET), age of mother at subject's birth, rural birth, rural living, well water use, farming as an occupation, exposure to pesticides, head tremor, exposure to general anaesthesia and to ionizing radiations, food restriction, concentration camp imprisonment and smoking has been assessed by using univariate and multivariate statistical techniques. RESULTS: In the conditional multiple logistic regression analysis, positive family history of PD (OR 41.7, 95% CI 12.2-142.5, P < 0.0001), positive family history of ET (OR 10.8, 95% CI 2.6-43.7, P < 0.0001), age of mother at subject's birth (OR 2.6, 95% CI 1.4-3.7, P=0.0013), exposure to general anaesthesia (OR 2.2, 95% CI 1.3-3.8, P=0.0024), farming as an occupation (OR 7.7, 95% CI 1.4-44.1, P=0.0212) and well water use (OR 2.0, 95% CI 1.1-3.6, P=0.0308) exhibited a significant positive association with PD, whereas smoking showed a trend toward an inverse relationship with PD (OR 0.7, 95% CI 0.4-1.1, P < 0.06). CONCLUSIONS: We conclude that both familial and environmental factors may contribute to PD aetiology.     

A meta-analysis of Parkinson's disease and exposure to pesticides

This study examined the association between Parkinson's disease (PD) and exposure to pesticides. A series of meta-analysis of peer-reviewed studies were performed, using 19 studies published between 1989 and 1999. Prior to the meta-analysis, all studies were reviewed and evaluated for heterogeneity and publication bias. Significant heterogeneity among studies was detected and combined odds ratio (OR) was calculated using the random effect model. The majority of the studies reported consistent elevation in the risk of PD with exposure to pesticides. The combined OR studies was 1.94 [95% confidence interval (95% CI) 1.49-2.53] for all the studies, and 2.15 (95% CI 1.14-4.05) for studies performed in United States. Although the risk of PD increased with increased duration of exposure to pesticides, no significant dose-response relation was established, and no specific type of pesticide was identified. Our findings suggest that exposure to pesticides may be a significant risk factor for developing PD.     

Exposure to pesticide as a risk factor for depression: A population-based longitudinal study in Korea

BackgroundExposure to pesticides is associated with mental disorders, including depression, especially among occupationally exposed populations, such as farmers. The results of experimental studies ascribed the negative effects of pesticides on mental health to their neurotoxic and endocrine-disrupting activities.PurposeThis study aimed to investigate the association between the risk of depression and high- or low-level exposure to pesticides in a rural population.MethodsThis longitudinal study was performed in 2005–2008 (baseline) and 2008–2012 (follow-up) to evaluate the risk of depression among 2151 Korean adults. A standardized questionnaire was used to obtain information on depression upon self-reported exposure to pesticide based on the Center for Epidemiologic Studies Depression Scale. Logistic regression analysis was performed to evaluate the association between pesticide exposure and depression. We adjusted the data for age, cigarette smoking status, current alcohol use, monthly income, educational level, marriage status, and religion.ResultsAmong the individuals who reported depression, the number of participants who used pesticides was significantly higher than that who did not (N = 61 [7.2%] vs. N = 54 [4.2%], P = 0.003). A positive association was noted between >20-year period of pesticide use and depression (odds ratio [OR], 2.35; 95% confidence interval [CI], 1.41–3.88). Individuals who reported depression showed greater odds of being exposed to higher pesticide concentrations (OR, 2.33; 95% CI, 1.40–3.88) and experiencing pesticide poisoning (OR, 5.83; 95% CI, 1.80–18.86) than those who did not.ConclusionExposure to pesticides at a high concentration was found to be associated with depressive symptoms among Korean adults.     

Dose-dependent protective effect of coffee, tea, and smoking in Parkinson's disease: a study in ethnic Chinese

INTRODUCTION: Few studies have examined the relationship of coffee and tea in Parkinson's disease (PD). The potential protective effect of coffee intake and risk of PD has not been studied in a Chinese population. There is a high prevalence of caffeine takers among Chinese in our population. OBJECTIVE: We undertook a case control study to examine the relationship between coffee and tea drinking, cigarette smoking, and other enviromental factors and risk of PD among ethnic Chinese in our population. METHODS AND RESULTS: 300 PD and 500 population controls were initially screened. Two hundred case control pairs matched for age, gender, and race were finally included in the analysis. Univariate analysis revealed significant association of PD with coffee drinking (p<0.0005), tea drinking (p=0.019), alcohol drinking (p=0.001), cigarette smoking (p<0.0005), and exposure to heavy metals (p=0.006). Conditional logistic regression analysis demonstrated that amount of coffee drunk (OR 0.787, 95%CI 0.664-0.932, p=0.006), amount of tea drunk (OR 0.724, 95%CI 0.559-0.937, p=0.014), number of cigarettes smoked (OR 0.384, 95%CI 0.204-0.722, p=0.003), history of heavy metal and toxin exposure (OR 11.837, 95%CI 1.075-130.366, p=0.044), and heart disease (OR 5.518, 95%CI 1.377-22.116, p=0.016) to be significant factors associated with PD. One unit of coffee and tea (3 cups/day for 10 years) would lead to a 22% and 28% risk reduction of PD. One unit of cigarette smoke (3 packs/day for 10 years) reduced the risk of PD by 62%. CONCLUSIONS: We demonstrated a dose-dependent protective effect of PD in coffee and tea drinkers and smokers in an ethnic Chinese population. A history of exposure to heavy metals increased the risk of PD, supporting the multifactorial etiologies of the disease.     

S18Y polymorphism in the UCH-L1 gene and Parkinson's disease: evidence for an age-dependent relationship.

We studied the relationship between Parkinson's disease (PD) and the S18Y polymorphism in the UCH-L1 gene and the effect on this relationship of age at onset, smoking, and pesticides. Patients requested free health coverage for PD to the Mutualité Sociale Agricole (MSA), the French health insurance organization for people whose work is related to agriculture. Controls requested reimbursement of health expenses to the MSA. A maximum of three controls were matched to each case. Analyses included participants with both parents born in Europe. There were no differences in S18Y genotypes between patients (n = 209; 67% SS, 32% SY, 1% YY) and controls (n = 488; 66% SS, 30% SY, 4% YY). The relationship between PD and S18Y was modified by age at onset (P = 0.03). The Y allele was inversely associated with PD for patients with onset before 61 years (odds ratio [OR] = 0.53; 95% confidence interval [CI], 0.29-0.99); there was no association for older patients (62-68 years: OR = 1.21; 95% CI, 0.67-2.20; >68 years: OR = 1.24; 95% CI, 0.67-2.31). Among patients, Y carriers had a later onset than noncarriers (P = 0.04). These findings were not modified or confounded by smoking and pesticides. In this community-based case-control study, carriers of the Y allele were at decreased risk of developing PD at a young age, independently of pesticides and smoking.     

Environmental factors and Parkinson's disease: a case-control study in the Tuscany region of Italy

To date the aetiology of Parkinson's disease (PD) is unknown although both genetic susceptibility and environmental factors appear to play an important role in the development of the disease. Recent data have also indicated that chronic exposure to a common pesticide can reproduce the neurochemical, behavioral and neuropathological features of PD. The epidemiological studies previously carried on the prevalence of PD in population exposed to environmental factors have produced controversial results, probably because of different trial design and different analysis methods. A case–control retrospective study was conducted in a well-defined geographic area in Tuscany—Italy with the aim to identify environmental factors possibly related to PD. No significant difference between PD patients and control subjects was observed in time spent in rural or industrial residence, in well water drinking and in the exposure to herbicides and pesticides. A significant difference between patients with PD and controls was reported for cigarette smoking, controls resulting more likely cigarette smokers in comparison with PD patients. The present findings support the view of a protective effect of cigarette smoking and do not show any significant association between environmental factors and the risk of development of PD.     

A pilot study of occupational and environmental risk factors for Parkinson's disease.

Increasingly, the etiology of Parkinson's disease (PD) has been linked to exposures to environmental toxicants. This epidemiologic pilot study used a self-administered questionnaire among 34 PD cases and 22 other neurology clinic control patients. All subjects were at least 40 years old. Risk factors investigated included occupation, well-water use, pesticide use, metal exposures, medical history, smoking, alcohol consumption, and drug use. Twenty-six percent of the male PD cases reported having been employed in farming versus eleven percent for male controls (OR = 3.1, 95% C.I. = 0.3 to 35). Sixteen percent of male cases versus none of the controls reported employment as welders. No clear trends involving exposure to either occupational or home pesticides emerged. In assessing occupational exposures to metals, aluminum and copper exposures tended to be more common among male cases than male controls. Additionally, as reported in other studies, smoking showed an inverse relationship with PD. Although the findings reported here are provocative, these results are statistically imprecise and must be interpreted cautiously because of the small number of subjects included in the study.     

Pesticides and risk of Parkinson disease: a population-based case-control study

BACKGROUND: Pesticide exposures are suspected risk factors for Parkinson disease (PD), but epidemiological observations have been inconsistent. OBJECTIVE: To investigate associations between pesticide exposures and idiopathic PD. DESIGN: Population-based case-control study. SETTING: Group Health Cooperative, a health care system in western Washington State, and the University of Washington. PARTICIPANTS: Two hundred fifty incident PD case patients and 388 healthy control subjects (age- and sex-matched). We assessed self-reported pesticide exposures using a structured interview. Odds ratios (ORs) and 95% confidence intervals (CIs) were determined using logistic regression models, controlling for age, sex, and smoking. RESULTS: Odds ratios for occupational exposures were not significant but suggested a gradient that paralleled occupational exposures (pesticide worker: OR, 2.07; 95% CI, 0.67-6.38; crop farmer: OR, 1.65; 95% CI, 0.84-3.27; animal and crop farmer: OR, 1.10; 95% CI, 0.60-2.00; and dairy farmer: OR, 0.88; 95% CI, 0.46-1.70). Odds ratios for organophosphates paralleled the World Health Organization hazard classifications, with parathion much higher than diazinon or malathion. We also found elevated ORs from herbicides (OR, 1.41; 95% CI, 0.51-3.88) and paraquat (OR, 1.67; 95% CI, 0.22-12.76). We found no evidence of risk from home-based pesticide exposures. We found significantly increased ORs from lifelong well water consumption (OR, 1.81; 95% CI, 1.02-3.21). CONCLUSIONS: The findings for occupational pesticide exposures are consistent with a growing body of information linking pesticide exposures with PD. However, the lack of significant associations, absence of associations with home-based exposures, and weak associations with rural exposures suggest that pesticides did not play a substantial etiologic role in this population.     

Comorbid cancer in Parkinson's disease

The aim of this article was to evaluate cancer occurrence before and after diagnosis of Parkinson's disease (PD). We investigated 692 patients newly diagnosed with PD and 761 age‐ and sex‐matched control subjects identified during two periods (1994–1995 and 2000–2003) within Kaiser Permanente Medical Care Program of Northern California. Primary cancers were searched and dated, and all participants were followed up until the end of membership, death, or December 31, 2008. We used unconditional logistic regression to evaluate the PD–cancer association before the date of PD diagnosis or the index date and Cox proportional hazards regression to evaluate the PD–cancer association after the index date. Nearly 20% (140 of 692) of the PD patients and 25% (188 of 761) of the non‐PD controls had ever had a cancer diagnosis. Before the index date, the prevalence of cancer was not significantly lower in patients with PD (8.1% PD vs. 9.2% controls; OR = 0.83; 95% CI 0.54–1.3). After the index date, the risk of developing a cancer did not differ between PD cases and controls (relative risk [RR] = 0.94; 95% CI 0.70–1.3). Among specific cancers, melanoma was more common among PD cases (before PD, OR = 1.5; 95% CI 0.40–5.2; after PD, RR = 1.6; 95% CI 0.71–3.6), but independent of dopaminergic therapy. Cancer occurrence is not significantly lower among patients with PD. The positive association between PD and subsequent melanoma merits further investigation, as it does not seem to be attributable to dopaminergic therapy, pigmentation, or confounding by smoking. © 2010 Movement Disorder Society.     

Lifestyle-related risk factors for Parkinson's disease: a population-based study

OBJECTIVES: To investigate the association of major lifestyle-related risk factors with the prevalent cases of Parkinson's disease (PD) identified by the Italian Longitudinal Study on Aging. METHODS: A total of 5632 individuals randomly selected from the population registers of eight centers were screened for parkinsonism using both a questionnaire and a neurologic examination. Screened positives underwent a structured clinical work-up for the diagnosis of parkinsonism and parkinsonism subtypes. RESULTS: We identified 113 prevalent cases of PD. Age, male gender, and pesticide-use license were significantly related to PD. Heavy smoking was inversely related to PD. Age (OR = 1.1; 95% CI, 1.06-1.15) and pesticide-use license (OR = 3.7; 95% CI, 1.6-8.6) kept their significant correlation with the disease in the multivariate analysis to adjust for all the variables under investigation. Multivariate analyses were made for men and women separately: pesticide exposure was positively associated with PD only in men. CONCLUSIONS: Pesticide exposure might represent a candidate for environmental factors involved in PD.     

Influence of coffee drinking and cigarette smoking on the risk of primary late onset blepharospasm: evidence from a multicentre case control study

Prior coffee and smoking habits were investigated in a multicentre case control study involving 166 patients presenting with primary late onset blepharospasm (BSP), 228 hospital control patients with primary hemifacial spasm and 187 population control subjects from five Italian centres. Information on age at disease onset, smoking and coffee drinking status at the reference age and average number of cups of coffee drunk/cigarettes smoked per day reached high and similar test-retest reproducibility in case and control patients. Unadjusted logistic regression analysis yielded a significant inverse association of prior coffee drinking and cigarette smoking with case status for the control groups. After adjustment for age, sex, referral centre, disease duration, years of schooling and ever coffee drinking/cigarette smoking, as appropriate, the smoking estimate lacked significance whereas the association of coffee intake and BSP did not (cases vs hospital control patients: OR 0.37 (95% CI 0.20 to 0.67); cases vs population control subjects: OR 0.44 (95% CI 0.23 to 0.85)). The strength of the inverse association between BSP and coffee intake tended to increase with the average number of cups drunk per day. There was a significant correlation between age of BSP onset and number of cups per day (adjusted regression coefficient 1.73; p = 0.001) whereas no correlation was found with number of packs of cigarettes per day. Coffee drinking may be inversely associated with the development of primary BSP and this association may partly depend on the amount consumed.     

Familial influence on parkinsonism in a rural area of Turkey (Kizilcaboluk-Denizli): a community-based case-control study.

This population-based study on parkinsonism in a genetically isolated community from a rural area of Turkey aimed to provide a selective evaluation of environmental and heritable risk factors. An increased prevalence of parkinsonism (4.1%) was detected in the village of Kizilcaboluk for people 65 years of age and older. This study included 36 patients with parkinsonism living in Kizilcaboluk and three times that number of age- and sex-matched people serving as controls. A questionnaire including demographic data, family history, education, occupation, data on exposures to pesticides, smoking, alcohol intake, and head trauma was administered. We found a significant association of parkinsonism cases with a positive family history in first-degree relatives (odds ratio [OR], 7.48; 95% confidence interval [CI], 2.52-22.17; P < 0.0001) and with pesticide exposure (OR, 2.96; 95% CI, 1.31-6.69; P = 0.015) compared to the control subjects. The value of genetically isolated populations for the identification of genetic risk factors for common and complex disorders has gained much attention recently because the genetic make-up of these populations is likely to be less complex than that of the general population and our findings should prompt investigations to the nature of a familial aggregation of parkinsonism in this population.     

Occupational exposure to manganese, copper, lead, iron, mercury and zinc and the risk of Parkinson's disease.

A population-based case-control study was conducted in the Henry Ford Health System (HFHS) in metropolitan Detroit to assess occupational exposures to manganese, copper, lead, iron, mercury and zinc as risk factors for Parkinson's disease (PD). Non-demented men and women 50 years of age who were receiving primary medical care at HFHS were recruited, and concurrently enrolled cases (n = 144) and controls (n = 464) were frequency-matched for sex, race and age (+/- 5 years). A risk factor questionnaire, administered by trained interviewers, inquired about every job held by each subject for 6 months from age 18 onward, including a detailed assessment of actual job tasks, tools and environment. An experienced industrial hygienist, blinded to subjects' case-control status, used these data to rate every job as exposed or not exposed to one or more of the metals of interest. Adjusting for sex, race, age and smoking status, 20 years of occupational exposure to any metal was not associated with PD. However, more than 20 years exposure to manganese (Odds Ratio [OR] = 10.61, 95% Confidence Interval [CI] = 1.06, 105.83) or copper (OR = 2.49, 95% CI = 1.06,5.89) was associated with PD. Occupational exposure for > 20 years to combinations of lead-copper (OR = 5.24, 95% CI = 1.59, 17.21), lead-iron (OR = 2.83, 95% CI = 1.07,7.50), and iron-copper (OR = 3.69, 95% CI = 1.40,9.71) was also associated with the disease. No association of occupational exposure to iron, mercury or zinc with PD was found. A lack of statistical power precluded analyses of metal combinations for those with a low prevalence of exposure (i.e., manganese, mercury and zinc). Our findings suggest that chronic occupational exposure to manganese or copper, individually, or to dual combinations of lead, iron and copper, is associated with PD.     

Parkinson's disease, smoking and family history

There is growing evidence that both genetic and environmental factors play a role in the etiology of Parkinson's disease (PD). The hypothesis of an interaction between genetic and environmental risk factors has been little explored, and never using a population-based case-control study design. Our objective was to investigate the possible interaction between smoking and family history in the etiology of PD, as a part of a collaborative population-based case-control study. We included 149 nondemented PD patients ascertained in three European prevalence surveys using a two-phase design. Each patient was matched by age (±2 years), gender, and center to three controls drawn from the same populations (n=375). Presence of PD among first-degree relatives and smoking history were assessed through an interview for 127 cased and 306 controls. In the overall sample we found suggestive evidence that family history and eversmoking interact in determining the risk of PD (P=0.09), with individuals exposed to both risk factors having the highest risk (OR=10.0; 95% CI=2.0–49.6). Analyses were repeated after stratification into two age-groups (cutoff: 75 years). In older patients, the joint exposure to both risk factors was associated with a significant increase in the risk of PD (OR=17.6; 95% CI=1.9–160.5). Among younger subjects, the OR for joint exposure was not significant. In conclusion, our findings suggest that smoking and family history interact synergistically on a multiplicative scale in determining the risk of PD in individuals older than 75 years. Received: 28 January 2000 / Received in revised form: 1 May 2000 / Accepted: 28 May 2000     

Synergistic effect of stromelysin-1 (matrix metallo-proteinase-3) promoter 5A/6A polymorphism with smoking on the onset of young acute myocardial infarction

The objective of this study was to elucidate the association between the polymorphism of stromelysin-1, also called matrix metalloproteinases-3 (MMP-3), and smoking in the pathogenesis of young acute myocardial infarction (MI). Plaque rupture is well established as a critical factor in the pathogenesis of acute MI. MMP-3 can degrade extracellular matrix and are identified extensively in human coronary atheroslcerotic plaques, and may contribute to the weakening of the cap and subsequent rupture. We studied 150 consecutive patients with acute MI onset at age under 45 years (84% men) and 150 sex- and age-matched control subjects. 5A/6A genotype in the stromelysin-1 promoter was determined using polymerase chain reaction and direct sequencing. Results show that the frequency of the 5A allele and the prevalence of 5A/5A + 5A/6A genotypes were both significantly higher in the young MI than the control group (35.0% vs. 20.0%, odds ratio [OR] 2.15, 95% confidence interval [CI] 1.30 to 6.80, p<0.001; 44.7% vs. 27.4%, OR 2.19, 95% CI 1.21 to 3.98, p=0.009). Multiple logistic regression analysis showed that the 5A allele was an independent risk factor (OR 2.36, 95% CI 1.24 to 5.90, p=0.008) as were as smoking (OR 3.92, 95% CI 1.75 to 9.21, p=0.001), diabetes mellitus (OR 3.51, 95% CI 1.41 to 6.32, p=0.0068) and hypertension (OR 1.85, 95% CI 1.35 to 4.33, p=0.0025) for the premature onset of MI. Compared to 6A/6A subjects, among patients who did not smoke, the 5A allele polymorphism was associated with a higher risk of MI at a young age (OR 2.69, 95% CI 1.3 to 8.6), but smoking carriers of the 5A allele had a significantly 10-fold higher risk of MI (OR 9.98, 95% CI 2.3 to 12.5). We can conclude that there was a significant association between the 5A/6A polymorphism in the promoter region of stromelysin-1 gene and young MI in Taiwan. A synergistic effect between smoking and this polymorphism for the premature onset of MI had been shown in this study.     

A family history of Parkinson's disease and its effect on other PD risk factors.

Parkinson's disease (PD) is likely a result of both inherited and exogenous factors. In a study of 144 PD cases and 464 controls, we used PD family history as a surrogate for inherited PD susceptibility. Cases were more likely to report a first- or second-degree relative with PD: 16.0 vs. 4.3%; odds ratio (OR) = 4. 2; 95% confidence interval (CI) = 2.3-7.6. A PD family history was a greater risk factor for PD in subjects under age 70 (OR = 8.8; 95% CI = 3.4-22.8) compared with those over 70 (OR = 2.8; 95% CI = 1.3-6. 1) and in men (OR = 8.1; 95% CI = 3.4-19.2) compared with women (OR = 2.6; 95% CI = 1.1-6.0). We also tested whether a PD family history modified the effects of other PD risk factors. In subjects with a PD family history, occupational exposure to copper, lead or iron increased the risk for PD (OR = 3.0; 95% CI = 0.7-13.3), but this was not the case for those without a family history (OR = 1.1; 95% CI = 0.7-1.6). Ever smoking cigarettes was inversely associated with PD in those without a PD family history (OR = 0.6; 95% CI = 0.4-0.9), but was positively associated with PD in those with a PD family history (OR = 1.7; 95% CI = 0.5-5.9). In summary, our results suggest that a PD family history, and perhaps, therefore, an inherited susceptibility, confers a greater risk for PD in men and individuals under 70 years of age and may modify the effects of environmental risk factors for PD.     

Chemical exposures and Parkinson's disease: a population-based case-control study.

The putative association between pesticide exposures and Parkinson's disease (PD) remains controversial. We identified all subjects who developed PD in Olmsted County, Minnesota, from 1976 through 1995, and matched them by age (+/- 1 year) and sex to general population controls. We assessed exposures to chemical products by means of telephone interview with cases, controls, or their proxies (149 cases; 129 controls). Exposure to pesticides related or unrelated to farming was associated with PD in men (odds ratio, 2.4; 95% confidence interval, 1.1-5.4; P = 0.04). The association remained significant after adjustment for education or smoking. Analyses for the other six categories of industrial and household chemicals were all nonsignificant. This population-based study suggests a link between pesticides use and PD that is restricted to men. Pesticides may interact with other genetic or nongenetic factors that are different in men and women.     

Risk factors for Parkinson's disease and impaired olfaction in relatives of patients with Parkinson's disease.

Our objective was to assess the association between risk factors for Parkinson's disease (PD) and abnormal olfaction in first-degree relatives of patients with PD. Factors including lower cigarette smoking and lower caffeine consumption have been associated with increased risk of PD. Idiopathic hyposmia has also been associated with an increased risk of PD. The relationship between risk factors for PD and impaired olfactory function has not been evaluated in relatives of PD patients. We conducted a mail survey of odor identification ability in 173 first-degree relatives of PD patients using the 40-item University of Pennsylvania Smell Identification Test (UPSIT). Respondents also completed a questionnaire inquiring about risk factors for PD including caffeine consumption, tobacco use, exercise, and exposures to heavy metals, well-water, and pesticides. There was a direct relationship between olfactory performance and lifetime caffeine intake. After adjustment for age, gender, and smoking status, subjects who reported drinking 2 to 3 cups of caffeinated beverages per day (2.6 points higher 95% CI: 0.5, 4.5) and 4 or more cups per day (3.7 points higher, 95% CI: 0.6, 6.7) had significantly better UPSIT scores than those who consumed less than 1 cup per day. There was no significant relationship between olfactory performance and other risk factors. In conclusion, abnormal olfaction is associated with significantly lower lifetime caffeine consumption in first-degree relatives of PD patients. Further research is warranted to determine whether a history of lower caffeine consumption confers additional risk for the development of PD in hyposmic relatives of PD patients.