Jeff Fowles

To quantify serum concentrations of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and dioxin-like compounds in former phenoxy herbicide production plant workers and firefighters, 20 years after 2,4,5-T production ceased. Of 1025 workers employed any time during 1969-1984, 430 were randomly selected and invited to take part in a morbidity survey and provide a blood sample; 244 (57 %) participated. Firefighters stationed in close proximity of the plant and/or engaged in call-outs to the plant between 1962 and 1987 also participated (39 of 70 invited). Reported here are the serum concentrations of TCDD and other chlorinated dibenzo-dioxins, dibenzofurans, and polychlorinated biphenyls (PCBs). Determinants of the serum concentrations were assessed using linear regression. The 60 men who had worked in the phenoxy/TCP production area had a mean TCDD serum concentration of 19.1 pg/g lipid, three times the mean concentration of the 141 men and 43 women employed in other parts of the plant (6.3...

The authors would like to acknowledge the contributions of Alan Fergusson, Andrew Ball, Chris Nokes, Liza Lopez, Ruth Pirie, Lou Gallagher (ESR); Mark Lyne (MAL Consultancy); Dr Greg Bodeker, Dr Richard McKenzie (NIWA); Chris Lewis, Tom O'Brien (NZHIS); Wayne ...

... Many valuable contributions from the GlobaLink internet-based public health community were received, with thanks to: Clive Bates, Neal Benowitz, Greg Connolly, Nina Jones, Barbara Langford, Murray Laugesen, and Stan Shatenstein. Page 5. ...

Background The Ministry of Health commissioned this scientific study to assess what level (if any) patrons in New Zealand bars are exposed to second-hand smoke (SHS), before and after changes to smoke-free legislation on 10 December 2004. The Smokefree ...

To measure secondhand smoke (SHS) levels in New Zealand bars prior to smokefree legislation enacted on 10 December 2004. Thirty bars were randomly selected from urban, surburban, and surrounding rural areas of Auckland, Wellington, and Invercargill. Bars were visited (on a Friday or Saturday night for a 3-hour stay between 1800 and 2400 hours) in July/August/September 2004 (winter) and again in October/November 2004 (spring). Each bar was visited by a group of 4 or 5 non-smokers participating in the study. All groups of participants spent a 3-hour block of continuous time in the bar. Saliva samples (approximately 0.5-2 mL) were provided immediately prior to entering the bar as well as 5-15 minutes after leaving the bar. Each group recorded the initial impression of air quality and ventilation, the number of observed lit cigarettes over three 10-minute intervals throughout the evening, and the number of patrons at each interval. In addition, any general comments about the venue (relevant to bar attendance or air quality on the evening) was recorded. Cotinine, the main metabolite of nicotine, was measured in saliva samples using Liquid Chromatography with tandem Mass Spectrometry (LC-MS-MS). In all bars, and in all volunteers, exposure to SHS was evident. Saliva cotinine increased after 3 hours in the bar (mean increase=0.66 ng/mL, SE=0.03 ng/mL, p value of <0.0001). The 30 bars randomly selected provided a good spectrum of SHS exposures, with mean cotinine increasing by approximately 8-fold. Smaller population centres showed greater exposures to SHS. A north-south gradient of exposure was also seen (highest exposures were in Southland). Higher exposures were seen in the winter than in the spring. The objective measures of SHS exposure correlated strongly with the volunteers' subjective observation of ventilation, air quality, and counts of lit cigarettes. One exception was where objective salivary markers indicated that even "seemingly smokefree" venues with "good ventilation" produced discernable levels of SHS exposure. We have utilised an objective, non-invasive scientific approach to assess SHS smoke exposure in patrons of New Zealand bars. Our results clearly indicate exposure to SHS, with regional and seasonal variation, prior to the introduction of smokefree legislation.

A broad definition of environmental medicine is the study of how the environment affects health, including the characterizing of exposures, and the practice of how to minimize any adverse effects. The term environmental medicine is effectively synonymous with the term environmental health, except that the latter term is often confused with “health of the environment,” so we will stick to the former term. The word environment also requires interpretation, because there are many subsets of environments that have special branches of environmental medicine associated with them. For example, occupational medicine (the study of the effects of the work environment on health) and social medicine (the study of the effects of social structures and dynamics on health). Of particular interest in this book are those aspects of the environment that relate directly to substances and processes of geological origin. This chapter will attempt to provide a brief outline of the principles and practice ...

To characterise the association between demographic and clinical factors and levels of total prostate specific antigen (tPSA) and its molecular derivatives complexed PSA (cPSA), free PSA (fPSA) and the ratio of free to total PSA (%fPSA)] in New Zealand Maori, Pacific Islanders and Europeans, in order to determine whether reported ethnic differences in PSA can be explained by lifestyle and social factors. Demographic and clinical factors were examined in relation to tPSA, fPSA and cPSA levels, in 1405 Maori, Pacific Island and New Zealand European men with no clinical evidence of prostate cancer, in the Wellington region of New Zealand. Any associations between levels of PSA and PSA derivatives and body mass index, smoking status, family cancer history, non-steroidal anti-inflammatory/vitamin supplement usage, number of sexual partners, age at first intercourse, previous vasectomy, marital/partnership status, educational level and socioeconomic status were investigated by backwards s...

To provide a hazard prioritisation for reported chemical constituents of cigarette smoke using toxicological risk assessment principles and assumptions. The purpose is to inform prevention efforts using harm reduction. International Agency for Research on Cancer Monographs; California and US Environmental Protection Agency cancer potency factors (CPFs) and reference exposure levels; scientific journals and government reports from the USA, Canada, and New Zealand. This was an inclusive review of studies reporting yields of cigarette smoke constituents using standard ISO methods. Where possible, the midpoint of reported ranges of yields was used. Data on 158 compounds in cigarette smoke were found. Of these, 45 were known or suspected human carcinogens. Cancer potency factors were available for 40 of these compounds and reference exposure levels (RELs) for non-cancer effects were found for 17. A cancer risk index (CRI) was calculated by multiplying yield levels with CPFs. A non-cancer...

BACKGROUND: Agricultural production frequently relies on the applications of pesticides that, under some circumstances, can be hazardous to human health. There is little known about the types and magnitude of agricultural pesticides applied near schools. Because of the potential public health risks to children, we examined the use of selected agricultural pesticides near public schools. METHODS: The California Environmental Health Tracking Program (CEHTP) assessed the use of agricultural pesticides near 2,511 public schools, attended by over 1.4 million students, from the top 15 agricultural counties in California for 2010. The accuracy and resolution of school parcel data were enhanced using geographic information systems (GIS) and satellite imagery. Enhanced school location data were linked with refined field-level pesticide application data to estimate agricultural pesticide use within ¼-mile of each school. Pesticides included in this study were selected for their public health ...

Hypo- or hyperthyroid states were induced in adult male mallards (Anas platyrhynchos) by subchronic exposure to daily injections of methimazole or a 9:1 ratio of thyroxine (T4): triiodothyronine (T3). The levels of T4 given were 0, 125, 250, or 500 micrograms/kg/day and for methimazole; 10 mg/kg/day for 22 or 21 days. Plasma T3 showed a lasting decrease with T4:T3 treatment, despite the attempt to maintain the normal T4:T3 ratio. Antibody formation to sheep red blood cells was decreased only at the 125 micrograms/kg/day dose of T4, and was unaffected by methimazole treatment. Natural killer cell activity to RP-9 tumor cells and macrophage phagocytosis of killed, opsonized Saccaromyces cereviseae were unaffected by treatment throughout the study. However, lectin-dependent cellular cytotoxic activity to RP-9 tumor cells was significantly decreased after 21 days of methimazole treatment, indicating that hypothyroidism may have an influence on cell-mediated immunity. Hypo- and hyperthyroid conditions had opposing effects on plasma cholesterol levels.

To determine whether age-adjusted levels of serum total (tPSA) and complexed (cPSA) prostate specific antigen and the ratio of free to tPSA (%fPSA) differ by ethnic group independent of symptomatic disease. The serum levels of tPSA, cPSA, and %fPSA in relation to age, ethnicity and obstructive urinary symptoms were examined in 1405 Maori, Pacific Island and New Zealand European men in the Wellington region of New Zealand, and indicative reference range estimates produced. Participants were non-randomly selected from two study populations. tPSA and cPSA increased with age while %fPSA decreased with age in all ethnic groups. Maori showed higher tPSA values in the 60-69 age group than other ethnic groups. cPSA increased more rapidly with age in Maori than in New Zealand Europeans or Pacific Islanders. %fPSA differed according to age across all three ethnic groups. The median and 5th percentile Pacific Island %fPSA values were higher in comparison to the %fPSA reference ranges of all other ethnic groups and were also higher than those reported in other studies. Once adjusted for urinary symptom score, only %fPSA in Pacific Island subjects remained significantly higher than that in New Zealand Europeans (P<0.001). Our study indicates that %fPSA differs by ethnicity independent of symptomatic prostate disease.

We investigated how mainstream smoke emissions vary and interrelate in 15 Australian and 21 Canadian brands, using public emissions disclosures from 2001. These disclosures provided emission data for 40 hazardous agents under both standard and intensive ISO testing conditions. Our analyses focused on "adjusted emissions" (i.e., emissions per milligram of nicotine yield) for 13 selected agents. Adjusted emissions differed significantly by ISO testing condition for 9 of the 13 selected agents. Intensive condition adjusted emissions were strongly negatively correlated for several agent pairs. Country and manufacturer variables were the strongest predictors of intensive condition adjusted emissions for 8 of the 13 selected agents and significant predictors for all of them. Taken together, these results suggest potential for the intent of emission limits to be undermined by risk swapping (in which one specific exposure is reduced within a group at the cost of another's exposure increasing) and risk shifting (in which a specific exposure is reduced within a group at the cost of that exposure's increasing within another group).

To describe the epidemiology and toxicology of poisoning deaths in New Zealand for 2001 and 2002. Poisoning mortality data for 2001 and 2002 were collected from the Coronial Service Office (CSO) as part of the New Zealand chemical injury surveillance system. There was 235 and 234 poisoning deaths in 2001 and 2002 respectively, an annual rate of 6.3 [95% CI of 5.5 to 7.1] deaths per 100,000 population for both years. Two-thirds (67.0%) of the deaths were intentional. The 25-44 year age group had the largest number of cases and highest age-specific rate (123 deaths, 11.1 [95% CI: 9.3-13.2] per 100,000 in 2001 and 119 deaths, 10.7 [(95% CI: 9.0-12.8] per 100,000 in 2002). Over two-thirds (68.9%) of the deaths were male. In 2001, the European rate was slightly higher than that for Maori but rates for the two ethnicities were similar in 2002. Geographically, West Coast District Health Board (DHB) had the highest rates. Rates increased with increasing deprivation. Nearly two-thirds (64.3%...

Polybrominated diphenyl ethers are manufactured for use as flame retardants in commercial plastics and textiles in Europe and North America. These studies investigated the acute and subchronic immunotoxicity and endocrine effects of a commercial pentabromodiphenyl either mixture, DE-71, in female C57BL/6 mice. Mice were orally exposed to acute single doses of DE-71 of 0, 0.8, 4.0, 20, 100, or 500 mg/kg, or to subchronic daily doses totaling 0, 250, 500, or 1000 mg/kg over a 14 day period. Immunotoxicity was assessed by measuring the plaque-forming cell response to sheep erythrocytes (SRBC) and natural killer cell (NKC) activity (basal and poly I:C stimulated) to YAC-1 target cells. Liver cytochrome P450 content and activities (ethoxyresorufin-o-deethylase (EROD) and pentoxyresorufin-o-deethylase (PROD)) as well as corticosterone (CS) and thyroxine (T4) concentrations were also measured. PROD activity was induced 3-5-fold in mice exposed acutely or subchronically to DE-71 at doses > 250 mg/kg. EROD activity and total microsomal cytochrome P450 content were significantly induced only in mice treated subchronically with DE-71; maximum induction of EROD was 3.3-fold. Total serum T4 concentrations were significantly lower in mice treated acutely with DE-71 at all doses except the 100 mg/kg dose. Total and free T4 concentrations were dose-dependently decreased in DE-71-treated mice following subchronic exposure. Plasma CS levels were elevated following subchronic exposure to DE-71. The elevation of CS was correlated with order of capture at necropsy, suggesting an interactive effect of DE-71 and stress. In regard to immunotoxicity, significant suppression of the anti-SRBC response was seen only in mice exposed subchronically to 1000 mg DE-71/kg, an exposure that also resulted in decreased thymus weight. NKC activity was not altered by exposure to DE-71.

Tertiary butyl alcohol (TBA) was administered to groups of 15 female B6C3F1 mice in drinking water at concentrations of 0, 2.0 or 20 mg TBA ml(-1), for 14 days, for assessment of gross and histological changes in the liver and thyroid, thyroid hormones (T3, T4, and TSH), total hepatic cytochrome P450 (Cyp) content, specific Cyp activities and quantitative PCR analysis of specific Cyp enzymes (Cyp1a1, Cyp2b9, Cyp2b10, Cyp3a11), sulfuryltransferases (ST1a1, ST2a2, and STn) and glucuronyltransferases (UGT1a1, UGT2b1, and UGT2b5). Phenobarbital (PB) was administered to a positive control group by oral gavage at a daily dose of 80 mg kg(-1). TBA caused, on day 14, a reduction in circulating T3 (12-15% decrease) and a dose-dependent reduction in T4 (13-22% decrease), with no evidence of thyroid pathology. Two of five livers examined in the 20 mg TBA ml(-1) dose group showed mild, diffuse centrilobular hypertrophy. On day 14, Cyp 7-benzoxyresorufin-O-debenzylase activity was significantly induced 12-fold by TBA at 20 mg ml(-1), and 1.8-fold at the 2.0 mg TBA ml(-1) concentration. Cyp 7-pentoxyresorufin-O-dealkylase activity was slightly induced (2.1-fold) by 20 mg TBA ml(-1) on day 14. Quantitative PCR analysis of gene transcripts showed a significant induction of Cyp2b10 and ST1a1 with both TBA concentrations, and a slight induction of Cyp2b9 at 20 mg TBA ml(-1) only. PB induced all phase I and phase II gene transcripts except for Cyp1a1 and Cyp2b9. These findings suggest that TBA, at and below doses used in chronic studies, is an inducer of phase I and phase II liver enzymes, with resulting decreases in circulating thyroid hormones in B6C3F1 mice.

An acute, whole-body inhalation study for allyl alcohol in Sprague-Dawley rats was designed to support derivation of AEGL values, with emphasis on establishing NOAELs for irreversible effects of different exposure concentrations and durations. Groups of 10 rats were exposed for 1 hour (0, 50, 200, or 400 ppm), 4 hours (0, 20, 50, or 100 ppm), or 8 hours (0, 10, 20, or 50 ppm). Clinical evaluations were performed during exposure and in an open field within 22-71 minutes after termination of exposure. Clinical pathology, gross necropsy, and histopathology (nasal tissues, larynx, trachea, lungs/bronchi, liver, and kidneys) were evaluated 14 days after exposure. Mortality was limited to 1 male exposed for 8 hours to 50 ppm. Clinical findings of gasping, rales, increased respiration noted at higher exposure levels were rapidly reversed. No treatment-related findings were observed in the liver and kidneys, or in the lungs of surviving animals. Histopathology in the nasal cavity was noted at all exposure levels following 1, 4, or 8 hours of exposure. Mild nasal inflammation was found at the lowest exposure levels (50-ppm/1-hour, 20-ppm/4-hour, and 10-ppm/8-hour). These effects were considered reversible and were not associated with related clinical signs. Severe, irreversible nasal olfactory epithelial lesions were present in 50 ppm/8-hour males. The NOELs for irreversible effects were 400-ppm/1-hour, 100-ppm/4-hour, and 20-ppm/8-hour. The incidence of severe findings was positively dependent on both concentration and the exposure duration. In contrast, the incidence of mild reversible findings did not appear to be dependent on duration.

Methods: The EHI's were developed using the DPSEEA (Driving force-Pressure-State-Exposure-Effect-Action) framework by linking existing environmental and health data at both national and local levels. This data was subsequently used to assess the feasibility [in ...