Radionuclides in cigarettes may lead to carcinogenesis via p16 inactivation

It is widely accepted that tobacco smoke is responsible for the vast majority of lung cancers worldwide. There are many known and suspected carcinogens present in cigarette smoke, including α-emitting radioisotopes. Epidemiologic studies have shown that increased lung cancer risk is associated with exposure to ionizing radiation, and it is estimated that the majority of smoking-induced lung cancers may be at least partly attributable to the inhaled and deposited radiation dose from radioisotopes in the cigarette smoke itself. Recent research shows that silencing of the tumor suppressor gene p16^INK4a (p16) by promoter methylation plays a role in smoking-related lung cancer. Inactivation of p16 has also been associated with lung cancer incidence in radiation-exposed workers, suggesting that radionuclides in cigarette smoke may be acting with other compounds to cause smoking-induced lung cancer. We evaluated the mechanism of ionizing radiation as an accepted cause of lung cancer in terms of its dose from tobacco smoke and silencing of p16. Because both radiation and cigarette smoking are associated with inactivation of p16, and p16 inactivation has been shown to play a major role in carcinogenesis, ionizing radiation from cigarette smoke likely plays a role in lung cancer risk. How large a role it plays, relative to chemical carcinogens and other modes of action, remains to be elucidated.     

Evaluation of the validity of the US EPA's cancer risk assessment of arsenic for low-level exposures: a likelihood ratio approach

Skin cancers associated with ingesting of arsenic have been documented since the 19th century. A study in the southwestern coastal area of Taiwan where people drank well water containing arsenic is generally recognised as providing the best data available for quantifying the risk, and the US Environmental Protection Agency (EPA) used these data to conduct a risk assessment of arsenic ingestion. However, the lowest exposure category in the Taiwan study included arsenic levels up to 290 µg L^–1, which is nearly six times higher than the current EPA maximum contaminant level (MCL), 50 µg L^–1. Therefore, the EPA risk assessment model extrapolated data on high-level exposures to generate risk estimates for low-level exposures. To evaluate the validity of this model, we conducted a quantitative review of epidemiological studies observing arsenic exposures below 290 µg L^–1. A ratio of the likelihood of the EPA model being inappropriate to that of it being appropriate was calculated for each study population as a measurement of the validity of the EPA model. Although existing human data on low-level exposures are limited, the review suggested that the EPA model is unlikely to be able to predict the risk of skin cancer accurately when the arsenic exposure level is between 170 and 270 µg L^–1.     

印染行业清洁生产技术

论述了目前印染行业水污染的现状及原因，指出调整产业结构、应用新工艺、大力提倡节约用水、清沽生产将是印染行业实现可持续发展的必由之路。     

Likelihood Ratio Analysis of Skin Cancer Prevalence Associated with Arsenic in Drinking Water in the USA

Several published studies have examined skin-cancer prevalence in regions of the USA that have concentrations of arsenic above the USA drinking-water standard. Those studies with adequate exposure and health outcome data did not report any skin cancer cases. Because the USA's arsenic concentrations are relatively low compared to some other countries and the study populations are small, the absence of reported skin-cancer cases could be due to an absence of risk in USA populations or random variability from a predicted risk. We used the current EPA arsenic cancer slope factor (CSF) model, which is derived from Taiwanese populations exposed to high levels of arsenic, to predict the expected number of skin cancers. We then conducted a likelihood ratio analysis, which showed that a null hypothesis (no additional skin cancer risk from arsenic) was approximately 2.2 times more likely than the hypothesis that ingested arsenic causes the predicted rate of skin cancers. Although based on small numbers, our analysis of USA populations indicates that the CSF derived from arsenic exposure in Taiwanese populations may be an overestimate when applied to USA populations.     

Particulate matter in new technology diesel exhaust (NTDE) is quantitatively and qualitatively very different from that found in traditional diesel exhaust (TDE)

Diesel exhaust (DE) characteristic of pre-1988 engines is classified as a "probable" human carcinogen (Group 2A) by the International Agency for Research on Cancer (IARC), and the U.S. Environmental Protection Agency has classified DE as "likely to be carcinogenic to humans." These classifications were based on the large body of health effect studies conducted on DE over the past 30 or so years. However, increasingly stringent U.S. emissions standards (1988-2010) for particulate matter (PM) and nitrogen oxides (NOx) in diesel exhaust have helped stimulate major technological advances in diesel engine technology and diesel fuel/lubricant composition, resulting in the emergence of what has been termed New Technology Diesel Exhaust, or NTDE. NTDE is defined as DE from post-2006 and older retrofit diesel engines that incorporate a variety of technological advancements, including electronic controls, ultra-low-sulfur diesel fuel, oxidation catalysts, and wall-flow diesel particulate filters (DPFs). As discussed in a prior review (T. W. Hesterberg et al.; Environ. Sci. Technol. 2008, 42, 6437-6445), numerous emissions characterization studies have demonstrated marked differences in regulated and unregulated emissions between NTDE and "traditional diesel exhaust" (TDE) from pre-1988 diesel engines. Now there exist even more data demonstrating significant chemical and physical distinctions between the diesel exhaust particulate (DEP) in NTDE versus DEP from pre-2007 diesel technology, and its greater resemblance to particulate emissions from compressed natural gas (CNG) or gasoline engines. Furthermore, preliminary toxicological data suggest that the changes to the physical and chemical composition of NTDE lead to differences in biological responses between NTDE versus TDE exposure. Ongoing studies are expected to address some of the remaining data gaps in the understanding of possible NTDE health effects, but there is now sufficient evidence to conclude that health effects studies of pre-2007 DE likely have little relevance in assessing the potential health risks of NTDE exposures.     

应用时间-活动模式估计儿童个体NOx暴露水平

将时间-活动模式与微环境空气污染物监测相结合估计儿童个体NO_x暴露水平. 分别在北京和青岛两市各选择3所学校监测校园环境污染物,并在每个学校选择10名儿童监测其家庭居室空气中ρ(NO_x)及个体24 h NO_x暴露水平,同时收集其时间-活动信息,采用时间-活动模式估计儿童的个体暴露水平. 交通工具中的NO_x暴露水平可通过校门口空气中ρ(NO_x)和交通工具的污染水平系数(λ)估计.结果表明:利用时间-活动模式模拟的儿童个体24 h NO_x暴露水平为0.041 mg/m3,与调整后的个体暴露实测水平相关性较好(R0.785,P<0.01),差值为(-0.002　6±0.013　0) mg/m3,二者的差异无统计学意义 (t0.139,P>0.05).表明采用时间-活动模式与微环境空气质量监测结果相结合方法估计的儿童NO_x暴露水平与个体实际暴露水平一致.