Assessment of wood smoke induced pulmonary toxicity in normal- and chronic bronchitis-like bronchial and alveolar lung mucosa models at air-liquid interface.

BACKGROUND: Chronic obstructive pulmonary disease (COPD) has the highest increased risk due to household air pollution arising from biomass fuel burning. However, knowledge on COPD patho-mechanisms is mainly limited to tobacco smoke exposure. In this study, a repeated direct wood smoke (WS) exposure was performed using normal- (bro-ALI) and chronic bronchitis-like bronchial (bro-ALI-CB), and alveolar (alv-ALI) lung mucosa models at air-liquid interface (ALI) to assess broad toxicological end points. METHODS: The bro-ALI and bro-ALI-CB models were developed using human primary bronchial epithelial cells and the alv-ALI model was developed using a representative type-II pneumocyte cell line. The lung models were exposed to WS (10 min/exposure; 5-exposures over 3-days; n = 6-7 independent experiments). Sham exposed samples served as control. WS composition was analyzed following passive sampling. Cytotoxicity, total cellular reactive oxygen species (ROS) and stress responsive NFkB were assessed by flow cytometry. WS exposure induced changes in gene expression were evaluated by RNA-seq (p ≤ 0.01) followed by pathway enrichment analysis. Secreted levels of proinflammatory cytokines were assessed in the basal media. Non-parametric statistical analysis was performed. RESULTS: 147 unique compounds were annotated in WS of which 42 compounds have inhalation toxicity (9 very high). WS exposure resulted in significantly increased ROS in bro-ALI (11.2%) and bro-ALI-CB (25.7%) along with correspondingly increased NFkB levels (bro-ALI: 35.6%; bro-ALI-CB: 18.1%). A total of 1262 (817-up and 445-down), 329 (141-up and 188-down), and 102 (33-up and 69-down) genes were differentially regulated in the WS-exposed bro-ALI, bro-ALI-CB, and alv-ALI models respectively. The enriched pathways included the terms acute phase response, mitochondrial dysfunction, inflammation, oxidative stress, NFkB, ROS, xenobiotic metabolism of AHR, and chronic respiratory disorder. The enrichment of the 'cilium' related genes was predominant in the WS-exposed bro-ALI (180-up and 7-down). The pathways primary ciliary dyskinesia, ciliopathy, and ciliary movement were enriched in both WS-exposed bro-ALI and bro-ALI-CB. Interleukin-6 and tumor necrosis factor-α were reduced (p < 0.05) in WS-exposed bro-ALI and bro-ALI-CB. CONCLUSION: Findings of this study indicate differential response to WS-exposure in different lung regions and in chronic bronchitis, a condition commonly associated with COPD. Further, the data suggests ciliopathy as a candidate pathway in relation to WS-exposure.

Clinical and morphological aspects of adenocarcinomas of the intestinal type in the inner nose: a retrospective multicenter analysis.

Clinical and histological parameters from 117 patients with wood dust-related sinonasal adenocarcinomas of intestinal type (ITAC) were analyzed and correlated with a follow-up period of 5 years at least. The rate of survival for 5 years was 53.1 % and for 10 years 30.2 %. Only 33 patients were free of disease. 74.2 % of patients with recurrences died in relation to ITAC. As expected, tumors of T4-category had the worst prognosis. The mucus content of a tumor was the most important histological parameter. Endonasal methods of surgery had no more positive survival rates after 5 years. An effect of radiotherapy has to be in discussion. The high incidence of tumor recurrences requires control examinations consistently.

Impact of exposure to wood dust on genotoxicity and cytotoxicity in exfoliated buccal and nasal cells.

Wood dust was classified by the IARC as a human carcinogen which causes sinonasal tumours. However, the exposure in different industries varies strongly and the risks of workers depend on the specific situation which can be assessed by the use of biomonitoring methods. The aim of this study was to investigate the workers who are exposed to low dust levels (below the permitted concentrations) with cytogenetic and biochemical methods. Micronuclei (MNi) which are indicative for genomic damage, nuclear buds which reflect gene amplification, binucleated cells which are caused by mitotic disturbances and acute cytotoxicity parameters (pyknosis, karyorrhexis, condensed chromatin, karyolysis) were monitored in buccal and nasal cells of workers of a veneer factory (n = 51) who are exposed to volatile wood-derived compounds, in carpenters of a furniture factory which use no synthetic chemicals (n=38) and in a control group (n = 65). Additionally, markers were measured in blood plasma which reflect inflammations (C-reactive protein, CRP) and the redox status, namely malondialdehyde (MDA) and oxidised low density proteins (oxLDL). No induction of micronucleated cells was observed in both epithelia in the two exposure groups while all other nuclear anomalies except pyknosis were increased; also one health-related biochemical marker (MDA) was significantly elevated in the workers. Taken together, the results of our study show that exposure to low levels of wood dust does not cause formation of MNi indicating that the cancer risks of the workers are not increased as a consequence of genetic damage while positive results were obtained in earlier studies with workers who are exposed to high dust levels. However, our findings indicate that wood dust causes cytotoxic effects which may lead to inflammations.

Indoor particulate matter in rural, wood stove heated homes.

Ambient particulate matter (PM) exposures have adverse impacts on public health, but research evaluating indoor PM concentrations in rural homes in the United States using wood as fuel for heating is limited. Our objectives were to characterize indoor PM mass and particle number concentrations (PNCs), quantify infiltration of outdoor PM into the indoor environment, and investigate potential predictors of concentrations and infiltration in 96 homes in the northwestern US and Alaska using wood stoves as the primary source of heating. During two forty-eight hour sampling periods during the pre-intervention winter of a randomized trial, we assessed PM mass (<2.5µm) and PNCs (particles/cm(3)) in six size fractions (0.30-0.49, 0.50-0.99, 1.00-2.49, 2.5-5.0, 5.0-10.0, 10.0+µm). Daily mean (sd) PM2.5 concentrations were 28.8 (28.5)µg/m(3) during the first sampling period and 29.1 (30.1)µg/m(3) during the second period. In repeated measures analyses, household income was inversely associated with PM2.5 and smaller size fraction PNCs, in particular. Time of day was a significant predictor of indoor and outdoor PM2.5 concentrations, and infiltration efficiency was relatively low (Finf (sd)=0.27 (0.20)). Our findings demonstrate relatively high mean PM concentrations in these wood burning homes and suggest potential targets for interventions for improving indoor air quality and health in rural settings.

Human urinary mutagenicity after wood smoke exposure during traditional temazcal use.

In Central America, the traditional temazcales or wood-fired steam baths, commonly used by many Native American populations, are often heated by wood fires with little ventilation, and this use results in high wood smoke exposure. Urinary mutagenicity has been previously employed as a non-invasive biomarker of human exposure to combustion emissions. This study examined the urinary mutagenicity in 19 indigenous Mayan families from the highlands of Guatemala who regularly use temazcales (N = 32), as well as control (unexposed) individuals from the same population (N = 9). Urine samples collected before and after temazcal exposure were enzymatically deconjugated and extracted using solid-phase extraction. The creatinine-adjusted mutagenic potency of urine extracts was assessed using the plate-incorporation version of the Salmonella mutagenicity assay with strain YG1041 in the presence of exogenous metabolic activation. The post-exposure mutagenic potency of urine extracts were, on average, 1.7-fold higher than pre-exposure samples (P < 0.005) and also significantly more mutagenic than the control samples (P < 0.05). Exhaled carbon monoxide (CO) was ~10 times higher following temazcal use (P < 0.0001), and both CO level and time spent in temazcal were positively associated with urinary mutagenic potency (i.e. P < 0.0001 and P = 0.01, respectively). Thus, the wood smoke exposure associated with temazcal use contributes to increased excretion of conjugated mutagenic metabolites. Moreover, urinary mutagenic potency is correlated with other metrics of exposure (i.e. exhaled CO, duration of exposure). Since urinary mutagenicity is a biomarker associated with genetic damage, temazcal use may therefore be expected to contribute to an increased risk of DNA damage and mutation, effects associated with the initiation of cancer.

Assessing the impact of national level interventions on workplace respiratory disease in the UK: part 2--regulatory activity by the Health and Safety Executive.

OBJECTIVE: To investigate whether interventions implemented by the UK Health and Safety Executive addressing exposure to isocyanate-based spray paints in motor vehicle repair (MVR), flour dust in craft bakeries, rosin-based solder flux fume (RBSFF) in the electronics industry, metalworking fluids and wood dust coincided with a decline in incidence of work-related short latency respiratory disease (SLRD) or asthma in the target groups. METHOD: Changes in the incidence of SLRD reported to a UK-based surveillance scheme were compared using a longitudinal, negative binomial regression model with ß distributed random effects. An interrupted time series design was used and comparisons according to inclusion or exclusion in the target group were made by including a statistical interactions expressed as a ratio of incidence rate ratios (RIRRs) in the model. RESULTS: The incidence of SLRD attributed to flour dust significantly increased relative to all other agents (RIRR: 1.10; 95% CI 1.06 to 1.16) whereas SLRD attributed to RBSFF significantly declined relative to all other agents (0.94; 0.90 to 0.99). No significant changes in the incidence of SLRD attributed to wood dust (1.03; 0.91 to 1.16) or spray paints (1.03; 0.95 to 1.11) relative to all other agents were observed. A higher proportion of reports originated from the industries targeted by the intervention for RBSFF (65/107; 61%) than spray painting (27/93; 27%) or wood dust (16/42; 38%). CONCLUSIONS: These data support a beneficial effect of interventions to reduce exposure to RBSFF but an increase in SLRD attributed to flour dust may indicate increased exposure or increased awareness of the problem.

[Adverse cutaneous reactions induced by exposure to woods]. / Niepozadane reakcje skórne spowodowane kontaktem z materialem drewnianym.

Various adverse cutaneous reactions may occur as a result of exposure to wood dust or solid woods. These include allergic contact dermatitis, irritant contact dermatitis and, more rarely, contact urticaria, photoallergic and phototoxic reactions. Also cases of erythema multiforme-like reactions have been reported. Contact dermatitis, both allergic and irritant, is most frequently provoked by exotic woods, e.g. wood of the Dalbergia spp., Machaerium scleroxylon or Tectona grandis. Cutaneous reactions are usually associated with manual or machine woodworking, in occupational setting or as a hobby. As a result of exposure to wood dust, airborne contact dermatitis is often diagnosed. Cases of allergic contact dermatitis due to solid woods of finished articles as jewelry or musical instruments have also been reported. The aim of the paper is to present various adverse skin reactions related to exposure to woods, their causal factors and sources of exposure, based on the review of literature.

Occupational asthma due to spruce wood.

Workers exposed to a variety of wood dusts are known to experience work-related respiratory symptoms, including occupational asthma. There are, however, few reports of occupational asthma due to spruce wood. We present the case of a 31-year-old sawmill owner with severe asthma caused by exposure to spruce wood dust, who developed asthmatic symptoms after 2 years of working. Investigations included clinical examination, routine laboratory tests, spirometry, chest X-ray, total serum immunoglobulin E (IgE) and specific serum IgEs against various woods and other occupational allergens. Additionally, we monitored the peak expiratory flow rate (PEFR) and symptom score both at work and when off work. Specific serum IgE for spruce wood was detected (7.8 IU/ml). The results of PEFR and workplace symptom-score monitoring, coupled with an elevated eosinophil count in induced sputum, supported the diagnosis of occupational asthma. To our knowledge, this is the first well-documented case of occupational asthma induced by spruce wood dust. A type I immunological mechanism seems to be responsible.

Lung cancer and occupation: A New Zealand cancer registry-based case-control study.

BACKGROUND: There are many proven and suspected occupational causes of lung cancer, which will become relatively more important over time, as smoking prevalence decreases. METHODS: We interviewed 457 cases aged 20-75 years notified to the New Zealand Cancer Registry during 2007-2008, and 792 population controls. We collected information on demographic details, potential confounders, and employment history. Associations were estimated using logistic regression adjusted for gender, age, ethnicity, smoking, and socio-economic status. RESULTS: Among occupations of a priori interest, elevated odds ratios (ORs) were observed for sawmill, wood panel and related wood-processing plant operators (OR 4.63; 95% CI 1.05-20.29), butchers (OR 8.77, 95% CI 1.06-72.55), rubber and plastics products machine operators (4.27; 1.16-15.66), heavy truck drivers (2.24; 1.19-4.21) and workers in petroleum, coal, chemical and associated product manufacturing (1.80; 1.11-2.90); non-significantly elevated risks were also observed for loggers (4.67; 0.81-27.03), welders and flame-cutters (2.50; 0.86-7.25), pressers (5.74; 0.96-34.42), and electric and electronic equipment assemblers (3.61; 0.96-13.57). Several occupations and industries not of a priori interest also showed increased risks, including nursing associate professionals (5.45; 2.29-12.99), enrolled nurses (7.95; 3.10-20.42), care givers (3.47; 1.40-8.59), plant and machine operators and assemblers (1.61; 1.20-2.16), stationary machine operators and assemblers (1.67; 1.22-2.28), food and related products processing machine operators (1.98; 1.23-3.19), laborers and related elementary service workers (1.45; 1.05-2.00), manufacturing (1.34; 1.02-1.77), car retailing (3.08; 1.36-6.94), and road freight transport (3.02; 1.45-6.27). CONCLUSIONS: Certain occupations and industries have increased lung cancer risks in New Zealand, including wood workers, metal workers, meat workers, textile workers and drivers. Am. J. Ind. Med. 54:89-101, 2011. © 2010 Wiley-Liss, Inc.

Medium-density fibreboard and occupational asthma. A case series.

BACKGROUND: Medium-density fibreboard (MDF) is a wood composite material, composed primarily of softwood, bonded with a synthetic formaldehyde-based resin. It is increasingly used, as it has various advantages over natural woods. METHODS: Enquiry of the national reporting scheme data and three case reports were used to further the evidence base linking this exposure to occupational asthma (OA). RESULTS: From 1991 to 2007, 21 cases of occupational sensitization to MDF were reported to the UK voluntary reporting scheme, Surveillance of Work Related Occupational Respiratory Disease (SWORD): 18 reported as occupational asthma (OA) and 3 as occupational rhinitis. All workers were male, with a mean age of 48 years, working in education, furniture manufacturing or joinery among other employments. CONCLUSIONS: Whilst reporting scheme data identified relatively small numbers of cases of OA likely to be due to MDF, the evidence base supporting this link is generally lacking. The three cases presented, where OA was attributed to MDF exposure, add to this evidence.

The reduction of dioxin emissions from the processes of heat and power generation.

The first reports that it is possible to emit dioxins from the heat and power generation sector are from the beginning of the 1980s. Detailed research proved that the emission of dioxins might occur during combustion of hard coal, brown coal, and furnace oil as well as coke-oven gas. The emission of dioxins occurs in wood incineration; wood that is clean and understood as biomass; or, in particular, wood waste (polluted). This paper thoroughly discusses the mechanism of dioxin formation in thermal processes, first and foremost in combustion processes. The parameters influencing the quantity of dioxins formed and the dependence of their quantity on the conditions of combustion are highlighted. Furthermore, the methods of reducing dioxin emissions from combustion processes (primary and secondary) are discussed. The most efficacious methods that may find application in the heat and power generation sector are proposed; this is relevant from the point of view of the implementation of the Stockholm Convention resolutions in Poland with regard to persistent organic pollutants.

Follicular B-Cell Lymphoma and Particulate Matter Associated with Environmental Exposure to Wood Dust.

BACKGROUND In humans, wood dust is a carcinogen. Indeed, a strong association between wood dust and lung cancer risk has been reported in woodworkers, as well as in the general population. CASE REPORT The patient was a 58-year-old man with follicular B-cell lymphoma. In the 10 years preceding the cancer diagnosis, he lived within 1/4 mile of a paper mill, where wood was processed. Computed tomography of the chest, abdomen, and pelvis revealed right hilar, mediastinal, abdominal, and retroperitoneal lymphadenopathy, bilateral pleural effusions, and a large soft-tissue mass infiltrating the small bowel mesentery. Analysis of the pleural fluid revealed the presence of a web of thin filopodia-like filaments, which trapped clusters of mesothelial cells and atypical lymphocytes. Single tubular filaments, morphologically similar to tunneling nanotubes, were seen originating from atypical lymphocytes and reaching neighboring cells. Furthermore, long, thick, cylindrical fibers of unknown nature, probably from the external environment, were also observed. CONCLUSIONS Because the patient lived in an unhealthy environment for many years, the possibility that his clinical condition was related to exposure to toxic emissions should be entertained. Considered in this context, the foreign fibers in his pleural fluid could be a direct consequence of inhalation of contaminants in the polluted air.

Indirect- and direct-acting mutagenicity of diesel, coal and wood burning-derived particulates and contribution of polycyclic aromatic hydrocarbons and nitropolycyclic aromatic hydrocarbons.

Particulates exhausted from two types of diesel engines (DEPs), burning-derived particulates from three types of coal (CBPs) and burning-derived particulates from three types of wood (WBPs) were separated into four fractions by silica-gel column chromatography using n-hexane, n-hexane-dichloromethane (3:1, v/v), dichloromethane and methanol, as the corresponding eluents. The indirect-acting mutagenicity of each fraction was assayed by the Ames test using the Salmonella typhimurium TA100 strain with S9 mix and the direct-acting mutagenicity was assayed using the S. typhimurium TA98 strain without S9 mix. The polycyclic aromatic hydrocarbons (PAHs) and nitropolycyclic aromatic hydrocarbons (NPAHs) of each fraction were determined by high-performance liquid chromatography (HPLC). Both direct- and indirect-acting of mutagenicities were the highest in samples of DEPs. The contributions of PAHs in samples of WBPs and NPAHs in DEPs were the largest, respectively.

A pilot survey of in-service home arsenic tracked in from chromated copper arsenate-treated decks.

Arsenic is a known carcinogen. It is also known to be readily dislodgeable from chromated copper arsenate (CCA)-treated lumber. The floors of in-service homes were tested for inorganic arsenic using a wipe method similar to the U.S. Housing and Urban Development (HUD) method for lead dust clearance sampling. Additionally, a hand-sampling method was used that involved direct dermal contact with the indoor floor surface. Amount of dislodgeable arsenic on the decks was highly correlated with arsenic concentrations on the indoor floors. Indoor arsenic concentrations were highest directly adjacent to the door. Concentrations in samples taken from the middle of rooms were less than half the concentrations of door samples, while concentrations in samples taken from untrodden floor space in the corners were mostly below the method detection limit. At a home without a CCA-treated deck, no measurable arsenic was found.

Toxicity evaluation of sappan wood extract in rats.

BACKGROUND: The heartwood of Caesalpinia sappan L. or sappan wood has long been used in folk medicines to treat tuberculosis, diarrhea, dysentery, skin infections and anemia. OBJECTIVE: To study the acute and subacute toxicities of sappan wood extract in rats. MATERIAL AND METHOD: For studying acute toxicity, a single oral dose of 5000 mg/kg of sappan wood was administered to rats. Subacute toxicity was studied by the daily oral administration of the extract at the doses of 250, 500 and 1000 mg/kg body weight for consecutive 30 days. RESULTS: The extract of sappan wood (5000 mg/kg) showed no toxicity in terms of general behavior change, mortality, or change in gross appearance of internal organs. Subacute toxicity study showed no abnormalities in treatment groups as compared to the controls. Body and organ weights, hematological, blood chemical, necropsy, and histopathological parameter of all groups were similar. CONCLUSION: Sappan wood extract did not produce any acute or subacute toxicity in both female and male rats.

Genetic damage in wood dust-exposed workers.

Exposure to wood dust is common in carpentry workshops. Wood dust is known to be a human carcinogen, with a very high relative risk of adenocarcinoma of the nasal cavities and paranasal sinuses. The goal of this investigation was to conduct genotoxicity monitoring of carpenters involved in wooden furniture industry in order to test possible wood dust-induced genotoxic effects due to occupational exposure. The level of genetic damage was determined by comet, micronucleus and chromosomal aberration (CA) assays in peripheral blood lymphocytes (PBL) of 60 carpentry workers. In addition, the micronucleus test in buccal epithelial cells was carried out in the same subjects. Total antioxidant enzyme activities were measured by the indices: superoxide dismutase, glutathione peroxidase and catalase. A group of 60 non-exposed subjects matched by age, smoking and alcohol consumption habits were chosen as controls. The effect of age, smoking, alcohol consumption and duration of exposure was also analysed in the subjects of the present study. The results showed a statistically significant increase in mean DNA damage by comet assay, micronuclei frequency in buccal cells as well as PBL and frequency of CA in the exposed workers when compared to controls (P < 0.05). Analysis of the data showed that all the confounding factors had a significant effect on DNA damage and micronucleus frequency in buccal epithelial cells and PBL. Smoking and alcohol consumption did not have any significant effect by chromosomal aberration test. Antioxidant enzyme levels significantly decreased in the exposed subjects. Our findings indicate enhanced levels of genotoxicity in carpenters. Hence, these workers may have an increased cancer risk.

Particles from wood smoke and traffic induce differential pro-inflammatory response patterns in co-cultures.

The inflammatory potential of particles from wood smoke and traffic has not been well elucidated. In this study, a contact co-culture of monocytes and pneumocytes was exposed to 10-40 microg/cm(2) of particles from wood smoke and traffic for 12, 40 and 64 h to determine their influence on pro-inflammatory cytokine release (TNF-alpha, IL-1, IL-6, IL-8) and viability. To investigate the role of organic constituents in cytokine release the response to particles, their organic extracts and the washed particles were compared. Antagonists were used to investigate source-dependent differences in intercellular signalling (TNF-alpha, IL-1). The cytotoxicity was low after exposure to particles from both sources. However, wood smoke, and to a lesser degree traffic-derived particles, induced a reduction in cell number, which was associated with the organic fraction. The release of pro-inflammatory cytokines was similar for both sources after 12 h, but traffic induced a greater release than wood smoke particles with increasing exposure time. The organic fraction accounted for the majority of the cytokine release induced by wood smoke, whereas the washed traffic particles induced a stronger response than the corresponding organic extract. TNF-alpha and IL-1 antagonists reduced the release of IL-8 induced by particles from both sources. In contrast, the IL-6 release was only reduced by the IL-1 antagonist during exposure to traffic-derived particles. In summary, particles from wood smoke and traffic induced differential pro-inflammatory response patterns with respect to cytokine release and cell number. Moreover, the influence of the organic particle fraction and intercellular signalling on the pro-inflammatory response seemed to be source-dependent.

Development of an obeche wood allergen quantification assay for the assessment of allergen exposure in workplaces.

OBJECTIVES: The purpose of this study was to develop a quantification assay to measure airborne concentrations of obeche wood allergen at workplaces. METHODS: Specific polyclonal antibodies to obeche wood were produced in rabbit and used to develop an inhibition enzyme immunoassay (EIA). Inhalable dust samples from three wood-processing companies were taken with a stationary sampling device (Gravicon VC25). The loaded dust filters were extracted under standardized conditions and measured with the assay. In addition, the antigen and allergen contents of obeche wood from different sources (Cameroon, N=5; Ghana, N=4) were analyzed from immunoblots, detected with rabbit immunoglobulin (Ig) G and human Ig E. RESULTS: Polyclonal antibodies specific for obeche wood allergens, without cross-reactivity to other woods, were used to establish the inhibition enzyme immunoassay. The assay is able to quantify allergen concentrations from 30 to 300 ng/ml. With inhibition enzyme immunoassay, exposure to airborne obeche wood allergen can be monitored in wood-processing companies. Inhalable dust samples from workplaces contained an average allergen concentration of 15 microg/g dust. Significantly lower protein and allergen contents were measured for obeche wood from Cameroon (ayous) in one company. IgE immunoblots indicated that the lower antigen and allergen contents of the ayous wood may be the result of its lacking the major obeche wood allergen, Trip s 1. CONCLUSIONS: The data showed that the total dust concentration in workplaces containing obeche wood dust did not correspond to the assessed allergen concentration. To estimate exposure limits regarding sensitization risk, it is necessary to measure the allergen content directly.