It has been suggested that dietary antioxidants reduce Parkinson's disease (PD) risk by neutralizing free radicals, thus preventing injury to neurons in the substantia nigra. This case-control study examined the possible role of long-term dietary antioxidant intake in PD etiology. Cases (n = 57) were males 45-79 years old with at least two cardinal signs of PD and no evidence of other forms of parkinsonism or dementia. Age-matched friend controls (n = 50) were chosen from lists provided by the cases. Usual dietary intake 20 years ago, including vitamins E and C and carotenoids, was assessed by a 102-item food frequency questionnaire. Odds ratios and 95% confidence intervals were calculated using conditional logistic regression. Antioxidant intake, adjusted for age, education, smoking, rural living, and total energy intake, was not associated with reduced PD risk. Trends toward greater PD risk were associated with higher intakes of vitamin C and carotenoids, especially xanthophylls, reflecting higher intakes by PD cases of fruit and certain vegetables. Intakes of sweet foods, including fruit, were associated with higher PD risk, suggesting that the observed trends may be due to a preference for sweet foods. This study does not provide support for a protective effect of long-term dietary antioxidant intake on PD risk.

Purpose To investigate indoor particulate matter (PM) level and various indoor air pollution exposure, and to examine their relationships with risk of lung cancer in an urban Chinese population, with a focus on non-smoking women. Methods We conducted a case-control study in Taiyuan, China, consisting of 399 lung cancer cases and 466 controls, of which 164 cases and 218 controls were female non-smokers. Indoor PM concentrations, including PM1, PM2.5, PM7, PM10 and TSP, were measured using a particle mass monitor. Unconditional logistic regression models were used to calculate odds ratios (ORs) and 95% confidence intervals after adjusting for age, education, annual income and smoking. Results Among non-smoking women, lung cancer was strongly associated with multiple sources of indoor air pollution 10 years ago, including heavy exposure to ETS at work (aOR=3.65), high frequency of cooking (aOR=3.30), and solid fuel usage for cooking (aOR=4.08) and heating (aORcoal stove=2.00). Housing characteristics related to poor ventilation, including single-story, less window area, no separate kitchen, no ventilator and rarely having windows open, are associated with lung cancer. Indoor medium PM2.5 concentration was 68ug/m3, and PM10 was 230ug/m3. PM levels in winter are strongly correlated with solid fuel usage for cooking, heating and ventilators. PM1 levels in cases are more than 3-time higher than that in controls. Every 10 ug/m3 increase in PM1 is associated with 45% increased risk of lung cancer. Conclusions Indoor air pollution plays an important role in the development of lung cancer among non-smoking Chinese women.

Inflammatory response is implicated as a biologic mechanism that links particulate matter (PM) air pollution with health effects. C-reactive protein (CRP), an important acute-phase reactant with profound proinflammatory properties, is used clinically as an indicator of the presence and intensity of inflammation. In vitro and in vivo animal studies suggest that CRP levels increase in response to PM exposure, but there was no consistency in epidemiologic studies. Herein, a systematic review was conducted to examine the association between PM exposure and serum CRP levels in humans. Elevated CRP levels were consistently found among children, and CRP elevations were also observed among healthy adults, albeit requiring higher peak levels of PM exposure. PM-induced CRP responses were not consistently found in adults with chronic inflammatory conditions, perhaps because of the use of anti-inflammatory medications in this population. Of the eight examined randomized trials, only one trial with a longer intervention period supported the effect of PM exposure on CRP concentrations. To provide conclusive evidence, further epidemiologic studies are needed to better quantify the magnitude of CRP level changes in response to PM with well-defined study populations and better control of various confounding factors.

Objective Green tea has been found to possess anti-inflammatory, anti-oxidative and anti-carcinogenic properties. The present study examines the association between green tea drinking and hepatocellular carcinoma (HCC) and its interactions with other risk or protective factors and single nucleotide polymorphisms (SNP) of inflammation and oxidative stress related genes. Methods A population-based case-control study with 204 primary HCC cases and 415 healthy controls was conducted in Taixing, China. Epidemiological data were collected using a standard questionnaire. SNPs of genes of the inflammation and metabolic pathways were genotyped at the UCLA Molecular Epidemiology Laboratory. Logistic regression was performed to estimate adjusted odds ratios and 95% confidence intervals. Results Longer duration and larger quantities of green tea consumption were inversely associated with primary HCC. Individuals who drank green tea longer than 30 years were at lowest risk (adjusted OR = 0.44, 95% CI: 0.19-0.96) compared with non-drinkers. A strong interaction was observed between green tea drinking and alcohol consumption (adjusted OR for interaction = 3.40, 95% CI: 1.26-9.16). Green tea drinking was also observed to have a potential effect modification on HBV/HCV infection, smoking and polymorphisms of inflammation related cytokines, especially for IL-10. Conclusion Green tea consumption may protect against development of primary HCC. Potential effect modifications of green tea on associations between primary HCC and alcohol drinking, HBV/HCV infection, and inflammation-related SNPs were suggested.

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