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Wood dust occupational hazard

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Wood dust occupational hazard

 

Another complex issue, for not all types of woods dust are equally hazardous.

Ohio State University Extension

Food, Agricultural and Biological Engineering

590 Woody Hayes Dr., Columbus, Ohio 43210

Wood Dust Exposure Hazards

AEX-595.1-2006 (Revised)

Thomas L. Bean, in collaboration with Timothy W. Butcher

Wood dust is created when machines are used to cut or shape wood materials. Industries that have a high risk of wood-dust exposure include sawmills, dimension mills, furniture industries, cabinet makers, and carpenters. Negative health effects have been associated with professions that shape, cut, or work wood. Companies need to be aware of the health effects of wood dust, as well as NIOSH and ACGIH exposure level recommendations and applicable OSHA standards, and how they may affect their production facility.

The terms hardwood and softwood have no reference to the actual hardness of the wood. Hardwoods are from deciduous broad-leafed trees, and softwoods are from conifers. A significant difference does exist in the effect of the dust created during their handling. Hardwoods such as oak, mahogany, beech, walnut, birch, elm, and ash have been reported to cause nasal cancer in wood-workers. This is particularly true when exposures are high.

The American Conference of Governmental Industrial Hygienists (ACGIH) recognizes wood dust as a "confirmed" human carcinogen and recommends a limit of 1 milligram per cubic meter (mg/m3 ) for hardwoods and 5 mg/m3 for softwoods. At this time, OSHA regulates wood dust as a nuisance dust; however, OSHA strongly encourages employers to keep exposures to a minimum and to adopt the ACGIH levels. The maximum permissible exposure for nuisance dust is 15 mg/m3, total dust (5 mg/m3, respirable fraction).

Health Effects

Exposure to wood dust may cause external and internal health problems. Adverse health effects associated with wood dust exposure include dermatitis, allergic respiratory effects, mucosal and non-allergic respiratory effects, and cancer.

Allergic respiratory problems can be caused by wood dust. The chemicals in wood that are associated with allergic reactions are generally found in the inner parts or heartwood of the tree. A hypersensitivity reaction leading to asthma has been reported as a result of exposure to commonly used woods, including Western Red Cedar, Cedar of Lebanon, Oak, Mahogany, and Redwood. The asthmatic reaction is believed to be species-specific.

Dermatitis is also a common health hazard associated with exposure to wood dust. Wood, usually as sawdust or splinters, may affect the skin or mucous membranes by mechanical action or by chemical irritation and sensitization. Irritant reactions appear to be more common among lumber workers. The main population of workers who suffer from dermatitis-related problems are those who work in secondary wood product manufacturing facilities, although cases have been documented in sawmill workers.

Cancers have been associated with wood dust exposure. The National Institute for Occupational Safety and Health (NIOSH) considers both hardwood and softwood dust to be potentially carcinogenic to humans. The three types of cancers associated with wood dust exposure are nasal and sinus cavity cancer, lung and other cancers, and Hodgkin's disease. The wood and cancer relationship was studied by Milham (1974), who conducted a mortality study involving the AFL-CIO United Brotherhood of Carpenters and Joiners of America. This study supports the hypothesis that wood contains carcinogenic agents. The cancer mortality patterns found were:

  • Excess lung cancer in acoustical tile applicators and insulators.
  • Excess gastrointestinal cancer in pile drivers.
  • Excess leukemia lymphoma group cancers in millwrights, mill workers, and lumber and sawmill workers.
  • Excess lung and stomach cancer in construction workers with the greater excesses found in workers in major urban areas.

Hodgkin's disease has also been associated with wood dust. One study (Milham & Hesser, 1967), which examined 1,549 white males terminally ill with this disease, showed an association between Hodgkin's disease and wood dust exposure. Another study (Spiers, 1969) concluded that men working in wood industries in the eastern United States were at special risk for the disease, due principally to the carcinogenicity of pollen grains from eastern pine species.

Western Red Cedar occupies a particular place in hazard awareness because it contains the irritant chemical plicatic acid. Plicatic acid is most concentrated in western red cedar, but it is also found in significant quantities in eastern white cedar and japanese cedar. Plicatic acid is believed to be the causative agent in western red cedar dust-induced asthma and affects between 4 and 13.5% of exposed populations (Chan-Yeung, 1994).

Exposure Limits

When the Occupational Safety and Health Act was passed in 1970, PELs for about 400 different substances were incorporated into the Act and became law. In 1985 OSHA was petitioned by the United Brotherhood of Carpenters and Joiners of America of the AFL-CIO to create a standard to protect workers from wood-dust levels deemed unsafe by the union. The union's proposed standard for wood dust set exposure limits at 1 mg/m3 for hardwoods and 5 mg/m3 for softwoods. The Forest Industry contended that the union's request would cost wood products manufacturers up to $1.5 billion per year and would ultimately reduce the number of manufacturers in the wood industry. After reviewing the health evidence presented, OSHA's finding was that a PEL of 1 mg/m3 for hardwoods was not warranted.

OSHA does not have a specific PEL for wood dust. However, the National Institute for Occupational Safety and Health (NIOSH) has established a recommended exposure limit (REL) for wood dust, all soft and hardwoods except western red cedar, of 1 mg/m3 as a TWA for up to a 10-hour workday and a 40-hour workweek [NIOSH 1992].

The American Conference of Governmental Industrial Hygienists (ACGIH) has assigned wood dust, all soft and hardwoods except western red cedar, a threshold limit value (TLV) of 1 mg/m3 for certain hardwoods, such as beech and oak, and 5 mg/m3 for soft wood, as TWAs for a normal 8-hour workday and a 40-hour workweek and a short-term exposure limit (STEL) of 10 mg/m3 for soft wood, for periods not to exceed 15 minutes. Exposures at the STEL concentration should not be repeated more than four times a day and should be separated by intervals of at least 60 minutes [ACGIH 1994, p. 36].

The ACGIH has assigned western red cedar dust a TLV of 0.5 mg/m3 because of its suspected involvement as an asthmatic trigger and sensitizer [ACGIH 2004].

Compliance with the PELs is required as last amended, August 4, 1997.

Steps to Mitigate the Problem

Compliance with the PELs was initially achievable by means of using "any reasonable combination of engineering, administrative, and respirator control methods" (Department of Labor, 1989). However, after December 31, 1993, compliance required the implementation of engineering controls.

Engineering control methods should be implemented before considering any other type of control. As of December 31, 1993, administrative controls and personal protective equipment may no longer be used as a means to comply with PELs. Central exhaust ventilation is the primary engineering control method.

Central exhaust systems are usually designed for specific operations in which the wood dust is captured at the machines and conveyed through an overhead piping system to a collector. For indoor applications, these systems can be designed with a heat exchanger that returns the heat or conditioned air to the room.

Dust collectors for individual machines are usually more expensive and require more maintenance. Temporarily closing ducts that service equipment not in operation increases air flow to the rest of the hoods or vacuum devices. Adding a stronger fan to the system may be another solution.

A ventilation engineer can often recommend a number of modifications to improve the performance of a specific ventilation system. Small changes or modifications to an existing ventilation system will generally be less costly than replacing the system.

Process or operator enclosure is another engineering control method. Operator enclosure can be used where process equipment is operated from a remote or semi-remote location. An example of this is a sawmill where the headrig and resaw operators work effectively from an enclosure or booth. This type of engineering control is not feasible in many situations.

Process enclosures are commonly used to reduce the noise levels of a piece of machinery. A wooden box can be constructed around the piece of equipment with insulation installed on the inside to dampen the noise level. This type of enclosure can also be used to reduce wood dust levels. Caution must be taken when using this type of modification because of the potential for equipment overheating due to inadequate ventilation.

Administrative controls include good housekeeping procedures. The use of compressed air for cleaning dust off equipment and other surfaces contributes significantly to employee exposure to wood dust. The alternatives to the use of compressed air include sweeping or vacuuming. For controlling wood dust exposure, vacuuming is preferred. Due to cost, it may be difficult to justify vacuuming as a substitute for compressed air; but, by experimenting with different vacuum attachments, an industrial vacuum can be made very efficient. Vacuums can also be used as an alternative to sweeping and using compressed air for removing dust from employees' clothing.

Proper maintenance is another control method. The proper combination of machine, tool, and work piece and proper machine operation can prevent unnecessary dust emissions. Local exhaust ventilation and air cleaning systems should be designed and maintained to prevent the accumulation of wood dust and the recirculating of wood dust into the work place. The ventilation system should be inspected periodically for effective performance.

Another cause of poor dust collection is the open sides of some machines or the openings at the cutterheads, such as those found on molders. In this case, air is drawn in from the sides rather than over the cutterhead where dust can be effectively collected. Also, when the cutting tools become dull, the radius of the cutting edge increases, causing the cutting tool to rub and crush the wood fibers rather than severing them cleanly. Smaller particles and more respirable dust result from poor tool geometry.

Good maintenance should be a priority and may contribute to improved productivity as well as provide reductions in dust levels. Other good practices include maintaining clean workspaces, wearing protective clothing, and avoiding skin contact to help prevent allergic reactions. Rotating jobs, classified as an administrative control, can reduce the amount of exposure by not allowing employees to work a full eight-hour shift in a high-dust level area. However, the rotation of workers is not considered a favorable safety and health procedure by OSHA.

When effective engineering controls are not feasible or while they are being instituted, appropriate respirators may be used. OSHA mandates that a person may not be assigned the use of a respirator unless it has been determined that they are physically able to perform the work and use the equipment. A local physician will determine what health and physical conditions are pertinent. The respirator user's medical status must be reviewed periodically (for instance, annually). Employers who assign respirators to employees must follow procedures listed by OSHA in 29 CFR part 1910.134 for respirator use.

How to Find Out if You Have a Problem

There are a number of ways to check the work place for excessive airborne wood dust. A visual check may immediately identify a problem. Look for dust collecting on equipment, clothes, face, and hair and around the breathing zone of workers. This will help determine where the dust is created and how to mitigate the problem. Sweeping the floors may also be causing unnecessary airborne wood dust.

A clean work area during equipment operation is a good indication that wood dust levels are below OSHA PELs. However, the only way to be certain is to monitor the air for wood dust. Air sampling records documenting compliance may protect a company in the case of future liability claims. Air monitoring, using battery-powered vacuum pumps with filter cassettes, will provide factual information on air quality. Air samples should be collected by a qualified person to ensure correct sampling procedures and reliable results.

One potential problem may be the existing ventilation system not operating at full potential. Check for broken or leaking ducts, clogged airways, and full dust collection bins that may be restricting the air flow. The system may be outdated or undersized due to changes or expansion of production facilities. If this is the case, certain modifications may be made to bring it to current standards (American National Standard Institute standard Z33.1-1961). The ventilation system may be adequate, but if improperly fitted, it may not be intercepting all dust being produced.

Something as straightforward as equipment layout may also be a source of wood-dust problems. The rotating blades of a planer may throw dust and wood chips back toward the operator. In some situations, the back edge of the saw blade of a circular saw can create dust that may be directed by the guard and projected towards the operator. A crosscut saw usually creates a jet of dust that may be directed towards another workstation, creating higher levels of dust at that station. Evaluate the dust generation patterns of existing and planned equipment and arrange equipment in the shop to reduce any problems.

Employers should take note of employees' complaints of shortness of breath and whether employees have been missing work because of dust exposure. Employees' past work histories may reveal exposures to wood dust and other air contaminants in previous jobs. Past and present health records can be compared to determine any changes in the respiratory health of workers that might suggest the need for improvements.

References

Chan-Yeung, M. 1994. Mechanism of occupational asthma due to western red cedar (Thuja plicata). American Journal of Industrial Medicine 25:13-8.

Department of Labor. Jan. 1989. Federal Register, pp. 2528-2533. January.

Mazurkiewicz, Michael, M. S. and J. L. Festa, 1989. "Study Evaluates Wood Dust Exposure in U.S. Plants." Wood and Wood Products. p. 158. July.

Meola, A. March 1985. "Toxic effects of Wood Dust Exposure." Professional Safety.

Milham, S. 1974. "Mortality Experience of the AFL-CIO United Brotherhood of Carpenters and Joiners of America, 1969-1970: Division of Field Studies and Clinical Investigations." NIOSH Publication No. 74-129. NIOSH, Salt Lake City, Utah.

Milham, S. and Hesser, J. E. 1967. "Hodgkin's Disease in Woodworkers." Lancet, Vol 2: 136-137.

"National Forest Products Assn. and Inter-Industry Wood Dust Coordinating Committee Seminar Review." 1989. Wood and Wood Products, p. 166. July.

Spiers, P. S. 1969. "Hodgkin's Disease in Workers in the Wood Industry." Public Health Reports, 84(5): 385-388.

Reviewed by Dr. Curt Hassler, WVU; Dr. Wayne Maines, WVU; Dr. Thomas G. Carpenter, OSU; and Dr. Randall K. Wood, OSU.

Originally funded in whole or in part from Grant Number U05/CCU506070-02,"Cooperative Agreement Program for Agricultural Health Promotion Systems," National Institute for Occupational Safety and Health. Timothy W. Butcher, OSHA Program Coordinator; Thomas L. Bean, Safety Leader.


All educational programs conducted by Ohio State University Extension are available to clientele on a nondiscriminatory basis without regard to race, color, creed, religion, sexual orientation, national origin, gender, age, disability or Vietnam-era veteran status.

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http://monographs.iarc.fr/htdocs/monographs/vol62/wood.html

 

WOOD DUST
(Group 1)

 

 

For definition of Groups, see Preamble Evaluation.  (also pasted on word document)

VOL.: 62 (1995) (p. 35)

5. Summary of Data Reported and Evaluation

5.1 Exposure data

Wood is one of the world's most important renewable resources. At least 1700 million m3 are harvested for industrial use each year. Wood dust, generated in the processing of wood for a wide range of uses, is a complex substance. Its composition varies considerably according to species of tree. Wood dust is composed mainly of cellulose, polyoses and lignin and a large and variable number of substances of lower relative molecular mass which may significantly affect the properties of the wood. These include non-polar organic extractives (fatty acids, resin acids, waxes, alcohols, terpenes, sterols, steryl esters and glycerols), polar organic extractives (tannins, flavonoids, quinones and lignans) and water-soluble extractives (carbohydrates, alkaloids, proteins and inorganic material).

Trees are characterized botanically as gymnosperms (principally conifers, generally referred to as softwoods) and angiosperms (principally deciduous trees, generally referred to as hardwoods). Roughly two-thirds of the wood used commercially worldwide belongs to the group of softwoods. Hardwoods tend to be somewhat more dense and have a higher content of polar extractives than softwoods.

It is estimated that at least two million people are routinely exposed occupationally to wood dust worldwide. Nonoccupational exposure also occurs. The highest exposures have generally been reported in wood furniture and cabinet manufacture, especially during machine sanding and similar operations (with wood dust levels frequently above 5 mg/m3). Exposure levels above 1 mg/m3 have also been measured in the finishing departments of plywood and particle-board mills, where wood is sawn and sanded, and in the workroom air of sawmills and planer mills near chippers, saws and planers. Exposure to wood dust also occurs among workers in joinery shops, window and door manufacture, wooden boat manufacture, installation and refinishing of wood floors, pattern and model making, pulp and paper manufacture, construction carpentry and logging. Measurements are generally available only since the 1970s, and exposures may have been higher in the past because of less efficient (or non-existent) local exhaust ventilation and other measures to control dust.

The wood species used in wood-related industries vary greatly by region and by type of product. Both hardwoods and softwoods (either domestically grown or imported) are used in furniture manufacture. Logging, sawmills and plywood and particle-board manufacture generally involve use of trees grown locally. Most of the wood dust (by mass) found in work environments has a mean aerodynamic diameter of more than 5 m. Some investigators have reported that the dust generated in operations such as sanding and during the processing of hardwoods results in a higher proportion of smaller particle sizes, but the evidence is not consistent.

Within the furniture manufacturing industry, exposure may occur to solvents and formaldehyde in glues and surface coatings. Such exposures are usually greatest for workers with low or negligible exposure to wood dust and are infrequent or low for workers with high exposure to wood dust. The manufacture of plywood and particle-board may entail exposure to formaldehyde, solvents, phenol, wood preservatives and engine exhausts. Sawmill workers may also be exposed to wood preservatives and fungal spores. Exposures to chemicals in industries where other wood products are manufactured vary but are in many cases similar to those in the furniture manufacturing industry.

5.2 Human carcinogenicity data

The risk for cancer, and particularly cancer of the nasal cavities and paranasal sinuses, among woodworkers has been investigated in many epidemiological studies. Some of the studies provided specific information on cancer risk associated with exposure to wood dust, and those studies were given greatest weight in the evaluation.

Most of the available cohort and case-control studies of cancer of the nasal cavities and paranasal sinuses have shown increased risks associated with exposure to wood dust. These findings are supported by numerous case reports. Very high relative risks for adenocarcinoma at this site, associated with exposure to wood dust, have been observed in many countries, particularly in Europe. The lower risks observed in the studies in the United States may be due to differences in concentration or type of wood dust, but in one of these studies the more heavily exposed groups had significantly increased risks. A pooled analysis of 12 case-control studies revealed a clearly increasing risk with increasing estimated levels of exposure to wood dust, overall and in most individual studies. The excess appears to be attributable to wood dust per se, rather than to other exposures in the workplace, since the excess was observed in various countries during different periods and among different occupational groups, and because direct exposures to other chemicals do not produce relative risks of the magnitude associated with exposure to wood dust.

Adenocarcinoma of the nasal cavities and paranasal sinuses is clearly associated with exposure to hardwood dust; in several series of cases of adenocarcinoma from different countries, a high proportion of cases had been exposed to hardwood, and these findings were confirmed in several case-control studies as well. There were too few studies of any type to evaluate cancer risks attributable to exposure to softwood alone. In the few studies in which exposure was primarily to softwood, the risk for cancer of the nasal cavities and paranasal sinuses was elevated but considerably lower than that in studies of exposure to hardwood or to mixed wood types; furthermore, in the studies of exposure to softwood, exposure to hardwood could not clearly be ruled out. It is more difficult to attribute excess risk to any particular species of wood. The concentration of wood dust and the duration of exposure may also contribute to differences in the risks of workers exposed to different types of wood. These studies consistently indicate that occupational exposure to wood dust is causally related to adenocarcinoma of the nasal cavities and paranasal sinuses.

In studies of squamous-cell carcinoma of the nasal cavities and paranasal sinuses, smaller excesses were generally reported than for adenocarcinomas, and a pooled analysis of 12 case-control studies found no association with exposure to wood dust.

A number of case-control studies on nasopharyngeal cancer have reported an association with employment in wood-related occupations; however, confounding was not ruled out from these studies, and the largest study, from Denmark, in which exposure to wood dust was estimated, did not confirm the association. Case-control studies of laryngeal cancer consistently showed an association with exposure to wood dust or woodworking; however, cohort studies of woodworkers gave consistently negative results. Overall, these studies provide suggestive but inconclusive evidence for a causal role of occupational exposure to wood dust in cancers of the nasopharynx.

Studies of the association between exposure to wood dust and cancers of the oropharynx, hypopharynx, lung, lymphatic and haematopoietic systems, stomach, colon or rectum individually gave null or low risk estimates, gave inconsistent results across studies, and did not analyse exposure-response relationships. {The failure of studies to find an increased risk in other exposed tissues supports the conclusion that the risk factor is very low, or that there is another causal mechanism.  One study (below) suggests that the presence of silica in some wood might be the principle reason for nasopharyngeal cancer.  This study mentions methanol in beech wood.—jk).  The evidence for an association between exposure to wood dust and Hodgkin's disease was somewhat more suggestive, in that some case-control studies showed moderately high risks, but these results were not substantiated by the results of cohort studies or some of the well-designed case-control studies. In view of the overall lack of consistent findings, there is no indication that occupational exposure to wood dust has a causal role in cancers of the oropharynx, hypopharynx, lung, lymphatic and haematopoietic systems, stomach, colon or rectum.

5.3 Animal carcinogenicity data

Dust from beech wood was tested for carcinogenicity by inhalation and for enhancement of carcinogenicity when administered with sidestream cigarette smoke or formaldehyde in two studies in rats, or with N-nitrosodiethylamine administered by subcutaneous injection in two studies in hamsters. The studies did not show any significant carcinogenic or co-carcinogenic potential of beech wood dust, but each of the studies suffered from various kinds of limitations and had some inadequacies in reporting of data.

The mutagenic fraction of a methanol extract of beech wood dust was tested for carcinogenicity by skin application in one study in mice. Although a significant, dose-dependent increase in the incidence of skin tumours and a marginally significant, dose-dependent increase in the incidence of mammary tumours were observed, these results cannot be used in an evaluation of the carcinogenicity of wood dust per se.

In a preliminary study, beech wood dust was tested for local carcinogenicity by intraperitoneal injection in rats; no peritoneal tumours were reported.

5.4 Other relevant data

General knowledge of particle size indicates that wood dust can be deposited in human upper and lower airways, the deposition pattern depending partly on particle size. Heavy exposure to wood dust may result in decreased mucociliary clearance and, sometimes, in mucostasis. No data were available on clearance of wood dust from the lower airways.

Exposure to wood dust may cause cellular changes in the nasal epithelium. Increased frequencies of cuboidal metaplasia and dysplasia were found in some studies of workers exposed to dust from both hardwood and softwood. These changes can potentially progress to nasal carcinoma.

Impaired respiratory function and increased prevalences of pulmonary symptoms and asthma occur in workers exposed to wood dust, especially that from western red cedar.

There is little reliable information on the effects of wood dusts on the respiratory tract of rodents. One study in vitro showed that various wood dusts are cytotoxic and can induce drug metabolizing enzymes.

Constituents of beech that can be extracted with polar organic solvents are genotoxic, as demonstrated by the induction of point mutations in bacteria, DNA single-strand breaks in rat hepatocytes in vitro and micronuclei in rodent tissues in vivo. Extracts of oak wood showed similar activity, but fewer data were available. Extracts of spruce, the only softwood tested, gave consistently negative results.

5.5 Evaluation

There is sufficient evidence in humans for the carcinogenicity of wood dust.

There is inadequate evidence in experimental animals for the carcinogenicity of wood dust.

Overall evaluation

Wood dust is carcinogenic to humans (Group 1).

 

 

 

 

From woodweb at http://www.woodweb.com/knowledge_base/Health_hazards_of_wood_dust.html, a lumber industry website. 

Health hazards of wood dust      

Studies have shown that breathing wood dust can be hazardous to your health. 1998.

by Professor Gene Wengert

Q.
I have seen some comments on rec.woodworking about the dangers of breathing wood dust, but none have been very specific. I posted a specific question, but got no responses except one wise-guy who said, "Breathing wood dust is bad for you." Thanks a lot.

Could you give me some specific information, or point me to a good article? I am a woodturner who turns almost exclusively hardwoods native to Northeast Ohio: maple (several species), walnut, black cherry, pinoak. Some of what I turn is spalted: what are the specific dangers there? Just how careful do I have to be?

A.
Regarding the issue of wood dust, one must realize that it both a political and medical issue. The brief history of wood dust is that in
England a rare form of nasal cancer showed up in 2 studies (1965 and 1968) and the common denominator seemed to be furniture and cabinet workers, which was translated to wood dust. But the occurrence of the cancer was extremely small, so the study is somewhat questionable at best. Other European studies failed to show a connection. It is worth noting that England processed a large volume of tropical timbers.

In the late 1970s, the National Cancer Institute did a study and found 37 nasal cancers listed as the cause of death; 8 were furniture workers. In England, a follow-up study failed to find any workers who had nasal cancer, and who worked in a furniture factory after 1945.

What do we know about wood. There are several tropical species that have high silica content. This chemical often results in nasal irritation on many people. There are also many people allergic to dust, molds, and other chemicals in wood.

In the 70s and early 80s, several groups studied the cancer risk from dust. It was weak. Then in 1985, OSHA was prohibited from regulating wood dust under the "nuisance dust" standard. So, OSHA begins the process of regulating wood dust, with a standard in 1989 and a subsequent court ruling making it ineffective, and so it goes today.

The basis for OSHA's initial rules were: 1) the evidence of carcinogenicity of wood is inconclusive; 2) a maximum exposure of 5 milligrams per cubic meter is appropriate for the irritant effects of wood and worker comfort. There was some evidence that softwoods (esp. western red cedar) were worse than hardwoods. Other groups wanted 1 mg/cubic meter.

Hope this helps you decide whether you want to breath wood. I personally use a very good dust filter mask at all times.

Professor Gene Wengert is Extension Specialist in Wood Processing at the Department of Forestry, University of Wisconsin-Madison.

Click on Wood Doctor Archives to peruse past answers.

If you would like to obtain a copy of "The Wood Doctor's Rx", visit the Wood Education and Resource Center Web site for more information.

 

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