Blood cadmium determinants among males over forty living in Mexico City.

BACKGROUND: Mexico City has air, water and food pollution problems; however, human exposure to cadmium and its sources have not been described. OBJECTIVES: To determine the blood cadmium (BCd) level and its main exposure sources among males aged 40 years or older living in different areas of Mexico City. METHODS: After receiving informed consent, we interviewed 702 males aged ≥40 years to collect data on their sociodemographic characteristics, lifetime occupation, smoking history, and dietary habits, using a validated questionnaire. The BCd level (µg/L) was determined by atomic absorption spectrophotometry. RESULTS: The BCd mean level ±â€¯SD was 2.61 ±â€¯0.82 µg/L, and 20% of men reported a potential cadmium occupational exposure. After adjusting for age and other potential confounders, the main determinants of the BCd level were the current smoking status at interview, with low (ß≤8.5packs/year vs. non-smoker = 0.46; 95% CI: 0.28-0.64 µg/L; p < 0.01) and high (ß> 8.5 packs/year vs. non-smoker = 0.71; 95% CI: 0.56-0.87 µg/L; p < 0.01) smoking intensity, and living in the Center (ßCenter vs. South = 0.20; 95% CI: 0.02-0.37 µg/L; p = 0.02) or West area of the city (ßWest vs. South = 0.40, 95% CI: 0.21-0.58 µg/L; p < 0.001). Moreover, the potential dietary sources of BCd included: liver (ßYes vs. No = 0.13, 95% CI: 0.03-0.23 µg/L; p = 0.01), "Chorizo" (ß>1-3servings/month vs. No = 0.14, 95% CI: 0.01-0.26 µg/L; p < 0.001), sausage and ham. CONCLUSIONS: The BCd levels observed in this population are high and only similar to those observed in workers from a sanitary landfill area in Southern Thailand. Potential environmental Cd exposure sources, such as industrial activity and previous land use, in the West and Center areas of the city should be explored in detail, especially in vulnerable population groups, such as children.

Smoking and prostate cancer: a life course analysis.

BACKGROUND: Inconsistent associations between smoking status and prostate cancer (PC) could be due to exposure assessment error. Reconstructing smoking behaviors over the life course could reduce exposure assessment error. METHODS: As part of a case-control study, we identified 402 incident and histologically confirmed PC cases that were matched by age (±5 years) to 805 population controls. Through direct interview, we obtained information about: age at smoking onset, intensity and frequency of cigarette smoking at different life stages, and smoking cessation age. Smoking status at interview and average smoking index over the lifetime (packs/year) were estimated. Life course smoking patterns were obtained applying the k-means+ method for longitudinal data to the smoking index (pack/year) for each life stage. RESULTS: Two life-course smoking patterns were identified among ever smokers: "pattern A" characterized by males who reported low and constant smoking intensity (87.8%), and "pattern B" (12.2%) males with an initial period of low intensity, followed by an increase during the second period. Compared to never smokers, pattern B was associated with higher poorly differentiated PC, (OR 2.30; 95% CI 1.21-4.38). No association was observed with average smoking index. CONCLUSION: Life course smoking patterns seem to capture the smoking variability during life course and reduce the likelihood of reverse causation. Using this assessment strategy our findings support the potential role of tobacco smoking in PC, particularly poorly differentiated PC. Prospective studies with comprehensive smoking history during the lifetime are needed to confirm these findings.

Dietary inflammatory index and prostate cancer risk in a case-control study in Mexico.

Recent evidence suggests that a pro-inflammatory diet could be associated with prostate cancer (PC) risk. To evaluate the association between dietary inflammatory index (DII) and PC risk as well as aggressiveness, we conducted a case-control study in Mexico City. Cases were 394 individuals with incident, histologically confirmed PC, who were matched by age (±5 years) with 794 population controls. Dietary information was obtained through a semi-quantitative FFQ with a 3-year frame of reference before diagnosis, for cases, or interview, for controls. On the basis of twenty-eight food parameters, we estimated the energy-adjusted DII (E-DII). According to the Gleason score at diagnosis, PC cases were categorised as high (≥8), moderate (=7) and low (≤6) PC risk. Independent, unconditional logistic regression models adjusted for potential confounders were used to estimate PC risk and PC aggressiveness. There were no significant associations between overall PC risk and E-DII (OR3rd v. 1st tertile 1·18; 95 % CI 0·85, 1·63; P=0·33) or among men with high-risk PC (Gleason≥8) (OR 1·46; 95 % CI 0·88, 2·42; P=0·14). These results do not support the hypothesis that a pro-inflammatory diet is related to PC risk and PC aggressiveness. However, further studies with larger sample sizes, with sufficient statistical power and of varying designs should be conducted to address this hypothesis.