METHODOLOGY: The data show that the status of atmospheric environment in Malaysia, in particular in highly industrialized areas such as Klang Valley, was determined both by local and transboundary emissions and could be described as haze and non-haze periods.
RESULTS: During the non-haze periods, vehicular emissions accounted for more than 70% of the total emissions in the urban areas and have demonstrated two peaks in the diurnal variations of the aforementioned air pollutants, except ozone. The morning 'rush-hour' peak was mainly due to vehicle emissions, while the late evening peak was mainly attributed to meteorological conditions, particularly atmospheric stability and wind speed. Total suspended particulate matter was the main pollutant with its concentrations at few sites often exceeding the Recommended Malaysia Air Quality Guidelines. The levels of other pollutants were generally within the guidelines. Since 1980, six major haze episodes were officially reported in Malaysia: April 1983, August 1990, June 1991, October 1991, August to October 1994, and July to October 1997. The 1997 haze episode was the worst ever experienced by the country. Short-term observations using continuous monitoring systems during the haze episodes during these periods clearly showed that suspended particulate matter (PM10) was the main cause of haze and was transboundary in nature. Large forest fires in parts of Sumatra and Kalimantan during the haze period, clearly evident in satellite images, were identified as the probable key sources of the widespread heavy haze that extended across Southeast Asia from Indonesia to Singapore, Malaysia and Brunei. The results of several studies have also provided strong evidence that biomass burning is the dominating source of particulate matter. The severity and extent of 1997's haze pollution was unprecedented, affecting some 300 million people across the region. The amount of economic costs suffered by Southeast Asian countries during this environmental disaster was enormous and is yet to be fully determined. Among the important sectors severely affected were air and land transport, shipping, construction, tourism and agro-based industries. The economic cost of the haze-related damage to Malaysia presented in this study include short-term health costs, production losses, tourism-related losses and the cost of avertive action. Although the cost reported here is likely to be underestimated, they are nevertheless significant (roughly RM1 billion).
CONCLUSIONS: The general air quality of Malaysia since 1970 has deteriorated. Studies have shown that should no effective countermeasures be introduced, the emissions of sulfur dioxide, nitrogen oxides, particulate matter, hydrocarbons and carbon monoxide in the year 2005 would increase by 1.4, 2.12, 1.47 and 2.27 times, respectively, from the 1992 levels.
METHODS: A total of 335,060 women participating in the European Prospective Investigation into Nutrition and Cancer (EPIC) Study, completed a dietary questionnaire from 1992 to 2000, and were followed-up until 2010 for incidence of breast cancer. Hazard ratios (HR) of breast cancer by country-specific, as well as cohort-wide categories of beverage intake were estimated.
RESULTS: During an average follow-up of 11 years, 1064 premenopausal, and 9134 postmenopausal breast cancers were diagnosed. Caffeinated coffee intake was associated with lower risk of postmenopausal breast cancer: adjusted HR=0.90, 95% confidence interval (CI): 0.82 to 0.98, for high versus low consumption; Ptrend=0.029. While there was no significant effect modification by hormone receptor status (P=0.711), linear trend for lower risk of breast cancer with increasing caffeinated coffee intake was clearest for estrogen and progesterone receptor negative (ER-PR-), postmenopausal breast cancer (P=0.008). For every 100 ml increase in caffeinated coffee intake, the risk of ER-PR- breast cancer was lower by 4% (adjusted HR: 0.96, 95% CI: 0.93 to 1.00). Non-consumers of decaffeinated coffee had lower risk of postmenopausal breast cancer (adjusted HR=0.89; 95% CI: 0.80 to 0.99) compared to low consumers, without evidence of dose-response relationship (Ptrend=0.128). Exclusive decaffeinated coffee consumption was not related to postmenopausal breast cancer risk, compared to any decaffeinated-low caffeinated intake (adjusted HR=0.97; 95% CI: 0.82 to 1.14), or to no intake of any coffee (HR: 0.96; 95%: 0.82 to 1.14). Caffeinated and decaffeinated coffee were not associated with premenopausal breast cancer. Tea intake was neither associated with pre- nor post-menopausal breast cancer.
CONCLUSIONS: Higher caffeinated coffee intake may be associated with lower risk of postmenopausal breast cancer. Decaffeinated coffee intake does not seem to be associated with breast cancer.