The chemical composition of tobacco smoke has been extensively examined, and the presence of known and suspected carcinogens in such smoke has contributed to the link between tobacco smoking and adverse health effects. The consumption of marijuana through smoking remains a reality and, among youth, seems to be increasing. There have been only limited examinations of marijuana smoke, including for cannabinoid content and for tar generation. There have not been extensive studies of the chemistry of marijuana smoke, especially in direct comparison to tobacco smoke. In this study, a systematic comparison of the smoke composition of both mainstream and sidestream smoke from marijuana and tobacco cigarettes prepared in the same way and consumed under two sets of smoking conditions, was undertaken. This study examined the suite of chemicals routinely analyzed in tobacco smoke. As expected, the results showed qualitative similarities with some quantitative differences. In this study, ammonia was found in mainstream marijuana smoke at levels up to 20-fold greater than that found in tobacco. Hydrogen cyanide, NO, NO x , and some aromatic amines were found in marijuana smoke at concentrations 3-5 times those found in tobacco smoke. Mainstream marijuana smoke contained selected polycyclic aromatic hydrocarbons (PAHs) at concentrations lower than those found in mainstream tobacco smoke, while the reverse was the case for sidestream smoke, with PAHs present at higher concentrations in marijuana smoke. The confirmation of the presence, in both mainstream and sidestream smoke of marijuana cigarettes, of known carcinogens and other chemicals implicated in respiratory diseases is important information for public health and communication of the risk related to exposure to such materials.

Exposure to indoor radon has been determined to be the second leading cause of lung cancer after tobacco smoking. Canadian population risk of radon induced lung cancer was assessed in 2005 with the radon distribution characteristics determined from a radon survey carried out in the late 1970s in 19 cities. In that survey, a grab sampling method was used to measure radon levels. The observed radon concentration in 14 000 Canadian homes surveyed followed a log–normal distribution with a geometric mean (GM) of 11.2 Bq m–3 and a geometric standard deviation (GSD) of 3.9. Based on the information from that survey, it was estimated that ∼10 % of lung cancers in Canada resulted from indoor radon exposure. To gain a better understanding of radon concentrations in homes across the country, a national residential radon survey was launched in April 2009. In the recent survey, long-term (3 month or longer) indoor radon measurements were made in roughly 14 000 homes in 121 health regions across Canada. The observed radon concentrations follow, as expected, a log–normal distribution with a GM of 41.9 Bq m–3 and a GSD of 2.8. Based on the more accurate radon distribution characteristics obtained from the recent cross-Canada radon survey, a re-assessment of Canadian population risk for radon induced lung cancer was undertaken. The theoretical estimates show that 16 % of lung cancer deaths among Canadians are attributable to indoor radon exposure. These results strongly suggest the ongoing need for the Canadian National Radon Program. In particular, there is a need for a focus on education and awareness by all levels of government, and in partnership with key stakeholders, to encourage Canadians to take action to reduce the risk from indoor radon exposure.

The developmental and neurobehavioral effects of gestational and lactational exposure to a mixture of 14 polychlorinated biphenyls (PCBs) and 11 organochlorine pesticides was examined and compared against the commercial PCB mixture Aroclor 1254. The mixture was based on blood levels reported in Canadian populations living in the Great Lakes/St. Lawrence basin. Pregnant Sprague-Dawley rats were dosed orally with 0.013, 0.13, 1.3, or 13 mg/kg of the chemical mixture or 15 mg/kg of Aroclor 1254 from gestation day (GD) 1 to postnatal day (PND) 23. The highest mixture dose decreased maternal gestation and lactation body weight, and produced high mortality rates (80% overall) and reductions in offspring weight that persisted to adulthood. Aroclor 1254 produced smaller but persistent decreases in offspring weight without affecting maternal weight or offspring mortality. Aroclor 1254 and 13 mg/kg of the mixture produced comparable decreases in maternal and offspring serum T4 levels and comparable alterations to maternal thyroid morphology. Aroclor 1254 delayed the righting reflex and ear opening, accelerated eye opening, and reduced grip strength at PNDs 10-14. The mixture at 13 mg/kg delayed negative geotaxis in addition to delaying righting reflex and ear opening and reducing grip strength but had no effect on eye opening. Lower mixture doses (0.13 and 1.3 mg/kg) also delayed ear opening but affected no other parameters. Developmental exposure to the chemical mixture was found to be more toxic than exposure to Aroclor 1254 and produced a different profile of effects on early neurodevelopment. This PCB/organochlorine pesticide mixture affects mortality, growth, thyroid function, and neurobehavioral development in rodents.

As part of the program to investigate mixture effects of environmental pollutants, this study describes clinical, biochemical, and histopathological effects in rats perinatally exposed to a mixture of persistent organochlorine pollutants and methylmercury that simulates the blood contaminant profile of humans residing in the Canadian Arctic. Groups of pregnant rats were administered orally 0, 0.05, 0.5, or 5 mg/kg body weight (bw)/d of a reconstituted mixture of organochlorine pollutants (referred to as mixture hereafter) from gestational day (GD) 1 to postnatal day (PND) 23. Positive and vehicle controls were given Aroclor 1254 (Aroclor hereafter, 15 mg/kg bw) and corn oil (vehicle), respectively. After parturition, the pups were colled to 8 per litter on PND 4, and killed on PND 35, 77, or 350, when tissues were collected for analysis. Gestational and lactational exposure of rats to mixture up to 5 mg/kg bw produced adverse effects in the offspring, including growth suppression, decreased spleen and thymic weights, increased serum cholesterol and liver microsomal enzyme activities, lower liver retinoid levels, and histological changes in the liver, thyroid, and spleen. Histological changes in the liver consisted of hepatic inflammation, vacuolation, and hypertrophy, while alterations in the thyroid were characterized by hypertrophy and hyperplasia of follicles. The hepatic and thyroidal effects were mild even at the highest dose. The spleen showed a dose-dependent atrophy in the lymphoid nodules and periarteriolar lymphatic sheath regions. Aroclor produced effects similar to those seen in the highest mixture group. In summary, this study demonstrates that exposure to the reconstituted mixture at 5 mg/kg bw produced growth suppression, changes in organ weights, and biochemical and histopathological changes in liver, thyroid, and spleen. This study also demonstrated that the blood level in rats given the 5-mg/kg dose, where most of the effects were observed, is 100-fold higher than the blood level in the 0.05-mg/kg group, which is comparable to that found in humans living in the Canadian Arctic region.

Naturally occurring isotopes of radon in indoor air are identified as the second leading cause of lung cancer after tobacco smoking. Radon-222 (radon gas) and radon-220 (thoron gas) are the most common isotopes of radon. While extensive radon surveys have been conducted, indoor thoron data are very limited. To better assess thoron exposure in Canada, radon/thoron discriminating detectors were deployed in 45 homes in Fredericton and 65 homes in Halifax for a period of 3 months. In this study, radon concentrations ranged from 16 to 1374 Bq m(-3) with a geometric mean (GM) of 82 Bq m(-3) and a geometric standard deviation (GSD) of 2.56 in Fredericton, and from 4 to 2341 Bq m(-3) with a GM of 107 Bq m(-3) and a GSD of 3.67 in Halifax. It is estimated that 18 % of Fredericton homes and 32 % of Halifax homes could have radon concentrations above the Canadian indoor radon guideline of 200 Bq m(-3). This conclusion is significantly higher than the previous estimates made 30 y ago with short-term radon measurements. Thoron concentrations were below the detection limit in 62 % of homes in both cities. Among the homes with detectable thoron concentrations, the values varied from 12 to 1977 Bq m(-3) in Fredericton and from 6 to 206 Bq m(-3) in Halifax. The GM and GSD were 86 Bq m(-3) and 3.19 for Fredericton, and 35 Bq m(-3) and 2.35 for Halifax, respectively. On the basis of these results, together with previous measurements in Ottawa, Winnipeg and the Mont-Laurier region of Quebec, it is estimated that thoron contributes ∼8 % of the radiation dose due to indoor radon exposure in Canada.