|
|
|
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
|
|
|||
|
|
|||
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|||
|
|
|||
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
Of the 2,246 cases, 1,011 (45 percent) were definite, probable, or possible (Table 2), based on the likelihood that symptoms were related to pesticide exposure. This article summarizes pesticide cases investigated by DOH that occurred in non-agricultural settings. A future article will discuss agricultural cases.
From 1995 through 1999, DOH received reports of 482 cases of suspected pesticide-related illness occurring in the non-agricultural occupational environment. DOH classified 291 of these as definite (40), probable (129), or possible (122). The cases included 150 males and 141 females. The majority of individuals received medical care for their pesticide illness: 141 (86 percent) at emergency rooms, 72 at physicians' offices, and 38 at walk-in clinics. Two received advice from Washington Poison Center (WPC) and 37 did not seek medical care.
The 291 cases occurred in 30 of the 39 counties of Washington. Twice as many occurred in western Washington (197, or 68 percent) as in eastern Washington (93, or 32 percent). Forty-four percent occurred in the Puget Sound counties of King (69), Pierce(33), and Snohomish (25). In Eastern Washington, the counties with the most cases were Yakima(24), Spokane (20), Grant (14), and Benton (13).
The most common sites (45 percent) for non-agricultural occupational pesticide illness were office buildings; both commercial (69) and non-commercial (63) applicators were involved (Table 3). Homes were the second most common (20 percent) location. Exposures in homes resulted from both commercial (39) and non-commercial (19) applications.
|
|
||||
|
|
||||
| Location |
|
|
|
|
| Office Buildings |
|
|
|
|
| Homes/ Apartments |
|
|
|
|
| Industrial Sites |
|
|
||
| Parks/Golf Courses |
|
|
||
| Veterinary |
|
|
||
| Other |
|
|
||
| Total |
|
|
|
|
| *Limited to cases with illness classified by DOH as definitely, probably, or possibly due to pesticide exposure. | ||||
Examples of "no application, indirect exposure" include waste collection workers and thrift shop workers exposed to pesticide spills, and a pesticide spill in a freight carrier. Only one incident occurred at a school, which involved an office worker using an insecticide on indoor plants.
Of the 132 cases occurring in offices, 59 percent involved exposure to pesticide residue (Table 4). These cases resulted from indirect exposure to pesticide residue from applications made hours before workers returned to the office. Twenty-three percent of cases in offices involved direct applications. Forty-eight percent of cases in offices involved non-commercial applications.
|
|
||||||
|
|
||||||
|
|
|
|
|
|||
|
|
Non-Commercial | Commercial | Non-Commercial | |||
| Residue |
|
|
|
|
|
|
| Drift |
|
|
|
|
|
|
| Applications |
|
|
|
|
|
|
| Other |
|
|
|
|
|
|
| Total |
|
|
|
|
|
|
| *Limited to cases with illness classified by DOH as definitely, probably, or possibly due to pesticide exposure. | ||||||
Thirty-five of the 58 occupational cases in homes or apartments occurred during the application (Table 4). Sixteen cases involved residue or drift exposure. Nineteen occupational cases also occurred in the home when a homeowner made the application and a worker, such as a plumber or builder, was exposed to pesticides at the residence.
Occupationally, men (60) were more likely to be involved in incidents from pesticide applications and women (66), from pesticide residue or drift. The routes of exposure in pesticide illnesses are inhalation, dermal, ocular, and ingestion. Seventy-one percent (207) reported one route of exposure and 29 percent (83) reported multiple routes of exposure. Inhalation was the most frequently reported route of exposure and occurred in 74 percent of cases (216).
The majority (81 percent) of cases were considered to have a mild medical outcome (Table 5). These cases frequently involved eye irritation, headache, shortness of breath, cough, and nausea.
|
|
||||
|
|
||||
| Severity |
|
|
|
|
| Mild |
|
|
|
|
| Moderate |
|
|
|
|
| Severe |
|
|
|
|
| Total |
|
|
|
|
Fifty-five cases had moderate symptoms, and one was severe. Twenty-seven of the "moderate severity" cases occurred in the office, 11 in homes, and six on industrial sites. Twelve locations were unknown. The type of activity included applications (22), cleaning/fixing (3), drift (6), residue (14), accident (8), and other (3). A severe case involved a licensed applicator who inadvertently allowed his gloves to become saturated with insecticide.
From 1995 through 1999, 598 individuals were involved in pesticide-related non-agricultural and non-occupational incidents. Of these, a total of 270 cases were classified as definite (38), probable (84) or possible (148) (Table 6). More women (132, 65 percent) than men (71, 35 percent) over the age of 17 were involved in pesticide illness. Sixty-seven cases involved children less than 18 years of age. Among cases involving children ages 11-17, twice as many were males (9) as females (5). Gender was not a factor among children younger than age 11.
|
|
||||||
|
|
||||||
|
|
|
|
|
|
||
| Home | Commercial |
|
|
|
|
|
| Non-Commercial |
|
|
|
|
|
|
| Office | Commercial |
|
|
|
|
|
| Non-Commercial |
|
|
|
|
|
|
| Industrial Site |
|
|
|
|
|
|
| Unknown/ Other |
|
|
|
|
|
|
| Total |
|
|
|
|
|
|
| *Limited to cases with illness classified by DOH as definitely, probably, or possibly due to pesticide exposure. | ||||||
The counties reporting cases most frequently in western Washington were King (54), Pierce (31), Snohomish (22), and, in eastern Washington, were Spokane (25), Yakima (20), and Benton (15). The majority of non-occupational cases occurred in homes or apartments (83 percent), and involved non-licensed applicators (77 percent). See Table 6.
Most of the non-agricultural and non-occupational pesticide cases were caused by the pesticide's user, through exposure during the application (40 percent) or to residues (25 percent) (Table 6). Inhalation was the most frequently reported route of exposure and occurred in 64 percent of cases; 118 reported inhalation exposure alone and an additional 55 reported inhalation in combination with other routes of exposure. Dermal exposure (35) or in combination with other routes of exposure (59), accounted for 35 percent of the cases. Ocular exposure occurred in 43 cases or 16 percent of the total.
The majority (78 percent) of cases were considered to have mild medical outcomes (Table 7). The five definite or probable severe cases all occurred at home and involved three children and two adults. The activities associated with these exposures were applications, a spill, an accident, and ingestion by a toddler.
|
|
||||
|
|
||||
| Severity |
|
|
|
|
| Mild |
|
|
|
|
| Moderate |
|
|
|
|
| Severe 1 |
|
|
|
|
| Severe 2 |
|
|
|
|
| Total |
|
|
|
|
Illness due to exposure to pesticides is a serious public health issue. Pesticide-related illnesses reported to and investigated by the Washington State Department of Health were reviewed to better understand the circumstances surrounding exposure and resulting health effects. From 1995 through 1999, DOH investigated 482 non-agricultural occupational cases. Sixty percent were confirmed definite, probable or possible cases. These incidents occurred primarily in offices (45 percent) and homes (20 percent) and resulted from exposure to applications or residues. Sixty-three of the cases in offices involved non-commercial applications. Inhalation was the most common route of exposure (74 percent). Eighty-one percent of the cases had mild medical outcomes. One was severe.
In the non-agricultural non-occupational setting, DOH investigated 598 reported cases of pesticide illness. Forty-five percent (270) were confirmed definite, probable, or possible. The majority (83 percent) occurred in the home and involved non-licensed applicators. Inhalation was the most frequently reported route of exposure. The majority of cases (77 percent) were classified as mild, 20 percent were moderate, and 3 percent were severe. Sixty-seven cases involved children younger than 18 years old.
For more information, please contact
Jane C. Lee, PIRT coordinator at (425) 453-1340 or jane.lee@doh.wa.gov.
Amidst the flurry of the presidential pardons in the waning moments of the Clinton administration, the EPA had little generosity toward arsenic in drinking water. With publication of the January 22, 2001, Federal Register (the government's town crier for all rules and regulations), the longstanding 50 µg/L (ppb) maximum contaminant level (MCL) for arsenic was lowered to 10 ppb (11). Congress had mandated EPA to propose a new drinking water regulation for arsenic as part of the reauthorization of the Safe Drinking Water Act in 1996. Furthermore, EPA was to seek research that would help reduce the uncertainty in assessing health risks from exposure to low levels of this naturally occurring, ubiquitous element.
Although the stricter arsenic MCL would not be effective until January 2006, the Bush administration wasted no time in canceling the rule until further review, a move applicable to numerous last-minute regulations imposed by the preceding administration. This cancellation was perceived by some to represent a putative "poison policy" on the part of the new President. A litany of diatribes subsequently flooded the mass media. Experts on drinking water standards were called upon to investigate the matter.
Unfortunately, many of these experts seemed to have political agendas that left the listening public more informed about the divisive nature of partisan politics than about the rationale behind a fivefold drop in the maximum contaminant level for arsenic. To hear the advocates present their case, one would think that the issue was more about big, bad, greedy polluters than about a natural element that we are all exposed to, whether we like it or not.
The real story, which I reveal below, is about the basis for lowering the arsenic standard and the likelihood the new standard would actually protect our health. In this story, the public can learn the extent to which mathematical models are driving policy decisions and gain insight about how EPA (and presumably other government agencies) determines the costs and benefits of regulations.
The political operatives were spinning the proposed hold on the old arsenic MCL as "kiddy poisoning," but the fact is that the drinking water standard had been 50 ppb since its inception by the Public Health Service in 1942 (12). EPA formalized the standard in 1975 under the National Interim Primary Drinking Water Regulation, which was mandated by the Safe Drinking Water Act (SWDA) (2, 12). The 50-ppb standard was based on the acute or short-term toxicity for possible high levels of exposure to arsenic in food and water.
Based on experiences with medicines containing arsenic and epidemiological reports from several countries (Taiwan, Chile, Argentina), the highly respected International Agency for Research on Cancer (IARC) declared arsenic a human carcinogen in 1980 (29). EPA followed suit in the mid-1980s, but the drinking water standard was not changed. Instead, EPA established a water quality criterion of 0.018 ppb under the aegis of the Clean Water Act. The water quality criterion was a guideline for discharges of point-source contaminants (e.g., from factories or mines) into all navigable (surface) waters, which may or may not be sources of drinking water. In contrast to the long-established drinking water standard, the water quality criterion was based on a formal risk assessment process emanating from a 1988 analysis of Taiwanese skin cancer data (12). The remarkably low criterion EPA adopted was pure risk management and designed to protect against one excess case of skin cancer per million people (a probability of 0.0001%).
The World Health Organization was the first agency to blink when, in 1993, it lowered its recommended drinking water standard from 50 ppb to 10 ppb (35). The European Union mandated its members to follow suit and now numerous countries have standards less than 50 ppb (37).
Realizing a serious discrepancy (and confusion) between the water quality criterion of 0.018 ppb and the MCL of 50 ppb, the EPA had been telegraphing for years that it desired to lower the MCL for arsenic (12). With the Congressional mandate to "fix" the drinking water standard, EPA commissioned the National Research Council (NRC), an independent research arm of the National Academy of Sciences, to advise them on the adequacy of the risk assessment models they planned to use to justify any actions to lower the standard.
Following the release (and blessing) of the NRC report in 1999 (27), EPA released its proposal to lower the arsenic drinking water standard (9). Under the SDWA, EPA must propose a maximum contaminant level goal (MCLG) for each primary drinking water contaminant (12). The MCLG is strictly health-based and should incorporate a safety factor. For carcinogens, EPA policy dictates an MCLG of zero. The MCL should be set as close as possible to the MCLG, but of course in reality zero doesn't exist. Thus, in releasing its proposal in 2000, EPA was asking for comments on MCLs of 3, 5, 10, and 20 ppb. The final rule, barely meeting the required Congressional deadline, was an MCL of 10 ppb. Even this proposed MCL did not meet EPA's desired goal of no more than a 1 in 10,000 chance of one excess cancer.
Normally, EPA decides a chemical causes cancer because rats develop tumors after being practically inundated with the stuff. Rodents, however, are not good models for testing arsenic. They are not nearly as sensitive as humans; in fact, it's downright difficult to give them enough arsenic to produce tumors without killing them first.
Adding insult to lack of rat injury, arsenic in its various forms seems not to be mutagenic (27). Rather, in some unknown way, arsenic interferes with cellular processes involved with repair of DNA damage. Depending on dose, arsenic in human lymphocyte cell cultures has differential effects: at low doses DNA synthesis can be stimulated, but at high doses it is inhibited (23). Interference with DNA synthesis can result in chromosomal breakage that may lead over long periods of time to loss of cell growth control and eventually tumors. Stimulation of DNA synthesis can lead to proliferation of DNA carrying mutations. The implications of these effects are confusing, compounded by some authors' claims that arsenic may be essential in very low doses for animal health (2).
The recognized pathway for inorganic arsenic detoxification in animals occurs via enzymes known as methyl transferases that attach carbon- and hydrogen-containing methyl groups to arsenic. The transformation to the organic methylated form, which occurs most efficiently in the liver, facilitates the elimination of arsenic in the urine. Methylated forms of arsenic had been believed to be of low toxicity, but recent work with human cell cultures shows that even the methylated forms may induce DNA damage by some unknown mechanism (20, 22). Feeding rats at ridiculously high doses (1500 mg/kg) of methylated arsenic also resulted in lung-specific DNA damage (38).
Given that rats seem non-responsive to arsenic (unless you hit them on the head with a bottle of the stuff), we must turn to human exposure cases for assessing its health hazards. Much of what we know about human sensitivity to arsenic comes from observations of populations living in regions served by ground water having extremely high arsenic concentrations. In fact, the arsenic story is one of the very few where application of epidemiology to chemical exposures in the general population has actually helped definitively associate a wide variety of ailments with exposure to concentrations several fold above 50 ppb.
High levels of arsenic in drinking water had been known to cause skin lesions and a type of gangrene in the extremities known as blackfoot disease (BFD). Medical reports of skin cancer caused by ingestion of medicinal arsenic have been traced back to 1888, and breathing of arsenic-laced dust by copper smelter workers or agricultural workers using lead arsenate have been associated with cases of lung cancer (14, 25, 29).
However, the epidemiological associations between cancer and environmental exposures to a population at large were weak until publication in the late 1960s of a study about southwestern Taiwanese populations with a high prevalence of BFD and non-melanoma skin cancers (i.e., both basal and squamous cell carcinomas) (31). Over 90% of the wells in the subject area had naturally occurring arsenic levels of 150 ppb or greater. The highest incidences of skin cancer were seen in villages using wells with over 600 ppb arsenic. Elevated levels of skin cancer had also been studied in regions of Argentina and Chile (31). As in Taiwan, drinking water was contaminated with levels substantially greater than the current 50 ppb MCL.
Toxicologists universally agree that arsenic at high levels in drinking water causes skin cancer. The elevated prevalence of skin cancer coincides with BFD or other skin abnormalities. But non-melanoma skin cancer is infrequently fatal, so an urgency to change the MCL was not pushed until reports of elevated incidences in internal cancers started flowing out of Taiwan in the mid 1980s (4, 6). By the late 1990s, Taiwanese researchers had published a host of landmark papers on the relationship between internal organ cancers and arsenic exposure in southwestern Taiwan, the endemic BFD region (3, 5, 7, 36). Bladder cancer was the pathology most strongly associated with high levels of arsenic intake, but lung and liver cancer incidences were also elevated. A specific type of bladder cancer pathology known as transitional cell carcinoma was recently found in another high arsenic-laced-water region in northeastern Taiwan (8). Although each of the Taiwanese reports essentially studied the same affected population from different angles, their conclusions have been bolstered by similar cancer incidence reports from regions in Argentina and Chile with high levels of arsenic in drinking water and elevated incidence of arsenic induced skin diseases (17, 30).
If there is one point of agreement about arsenic, high levels of exposure in drinking water can cause cancer, and the bladder seems to be the most vulnerable site of attack (27). Like the predictable results from high-dose rodent cancer tests, humans exposed involuntarily to arsenic at extremely high levels (relative to what is typical) also get cancer. Unlike the rat studies, however, the dose levels are not carefully controlled nor actually measured on an individual basis.
Because over 98% of the U.S. population drinks water with arsenic below 20 ppb (9, 13), EPA has the dilemma of translating the human epidemiology data from high arsenic concentrations to low (and more typical) concentrations. Here is where complex mathematics and statistical modeling come into play. When you don't have data to cover low doses, you "reason" these data into existence by assuming that the risk of cancer (i.e., incidence of cancers relative to the whole population) is linear from high doses to low doses. In other words, zero exposure to arsenic results in a zero probability (or zero incidence) of bladder cancer and any incremental exposure above zero results in a directly proportional increase in risk. This model, known as the linear dose-response, assumes there is no threshold for cancer induction, regardless of exposure (Figure 1). EPA defaults to the no-threshold assumption when the mechanism of toxicity is unknown (9), despite evidence there may be a threshold. (Another form of this model is the linear-quadratic response curve, where cancer risk begins to increase faster than the incremental increases in dose. Such an effect has been observed in many of the Taiwanese epidemiological studies.)
|
|
|
|
 |
|
|
The no-threshold dose response has been widely criticized as being unrealistic (1, 15, 32). Some researchers maintain that at high concentrations of arsenic, the ability of the liver to detoxify it by methylation may be exceeded resulting in biochemical interactions not occurring at lower doses (1, 2). Other epidemiological studies do not support significantly increased risks for skin cancer or bladder cancer at doses less than several hundred ppb (15, 16). Studies of lower exposures to arsenic in the U.S. compared to southwestern Taiwan have failed to show elevated incidences of skin or bladder cancer (19, 21, 26, 33). Ten years ago, EPA's own Science Advisory Board recommended that the agency use a non-linear dose-response model to characterize risk (9). This model would allow minimal effects at very low doses, but for all practical purposes it is similar to the threshold model (Figure 1).
In its proposals for lowering the MCL, EPA seemed to dismiss any evidence that might support treating arsenic as if there were a threshold. Somehow this defies common sense in that we are continuously exposed to low levels of arsenic: our crops absorb arsenic from soils and drinking water always contains a greater-than-zero concentration of arsenic. To say there is no threshold is to say we are at increased risk for cancer when we eat fruit, vegetables, and cereal. I would hate to think Mom was wrong for telling me veggies were good for me.
In a follow-up discussion of its June 2000 proposal to change the MCL (10), the EPA highlighted a recently published paper (24) that tested several statistical models for re-analyzing the Taiwanese epidemiological data (6, 36) and computing the lifetime risk of dying from bladder cancer at different levels of arsenic exposure. The preferred model employed a technique known as Poisson regression and assumed no threshold in the dose-response curve. To make a long story short, EPA ran the models and presented its risk estimates for bladder and lung cancer at each of several proposed MCLs for arsenic in drinking water (Table 1).
|
|
||||
|
|
||||
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
| 1/ Assumes the incidence rate of cancer is the same as the death rate. | ||||
| 2/ Probabilities for MCLs 3-20 ppb based on (11); 50 ppb based on (24). | ||||
| 3/ Chances of not contracting cancer are calculated by subtracting the chance of contracting cancer from 100%. | ||||
At the current MCL there is a 0.33% chance of contracting bladder and lung cancer (Table 1). This chance can be thought of as the proportion of people in a specified population that might contract cancer or the chance an individual might contract it over their lifetime. If the standard were set to 10 ppb, the chance of contracting cancer would drop to 0.03%. While a tenfold decrease in the risk of cancer sounds very impressive, consider that the chance of not getting cancer is 99.67% and 99.97% at the 50 and 10 ppb MCL, respectively. In other words, the chances of not getting cancer from drinking arsenic-tainted water are pretty good even if the permissible level remains at 50 ppb.
How reliable is the estimate of a 0.33% combined chance of contracting bladder and/or lung cancer from drinking water with 50 ppb arsenic? Although the probability was estimated using a mathematical model because no reliable dose-response data exists in the United States, the question can be answered by examining current cancer rate statistics published by the National Cancer Institute. For example, in the database covering the years 1973-1996, the combined incidence/mortality of bladder and lung cancer was equivalent to a 0.126% chance of contracting those diseases (34). So, for the population covered by the database as a whole, the actual chance of contracting cancer was three times less than what EPA predicts would happen if they kept the current arsenic MCL at 50 ppb. Looking at risk more optimistically, a person has a 99.87% chance of not contracting lung or bladder cancer.
How do aging and cumulative exposure figure into the overall picture? If arsenic in water were contributing significantly to increases in bladder and lung cancer in the United States, then as the population aged and drank arsenic longer, it seems logical to predict increases in incidence of these cancers in older individuals. Indeed, the Taiwanese data for internal cancers shows big jumps in disease incidence in age groups 50 and above compared to younger age groups. While no comparable age-based studies have been conducted in the United States, it is important to note that the overall incidence of these cancers is decreasing, even as the median age of the population increases. In fact, the U.S. cancer statistics showed a 0.8% drop in incidence of bladder cancer and a 1.4% drop in incidence of lung cancer for the years 1990-1996. This is good news for all ages.
Finally, one advocacy organization, the Natural Resources Defense Council, stated erroneously that the NRC analysis indicated that one person out of 100 would get cancer from drinking arsenic in water at the current MCL (28). The NRC actually stated that a linear extrapolation of the dose-response curve for Taiwanese cancers would yield a combined bladder and lung cancer risk approaching one in 100. In other words, the risk could be 1%, unless of course you view the glass as half-full and see the chance of not getting cancer as 99%. Obviously, the NRDC has confused a risk estimate with real events. Of the total U.S. deaths, 540,000 were from all types of cancer, giving a probability of 0.2% (540,000 divided by 270 million U.S. residents), which is 2 deaths per 1000 people, clearly fivefold less than the very conservative risk estimate for arsenic-induced bladder and lung cancers. If a 0.2% chance of dying from cancer is scary, then consider that in the United States, in any given year, there is a 10% chance of dying from any cause (18).
How much will we pay to achieve a tenfold reduction in risk of contracting cancer (or a 0.3% improvement in the chance of not contracting cancer) by lowering the arsenic standard to 10 ppb? To estimate costs, EPA first examined the currently available feasible remediation technologies and assessed the expense of each (11). Next, they spread the cost around the country. The amount you are projected to pay depends on the size of your water system and where you live. Because the highest arsenic levels are clustered in the west and the northeast (9), residents of those states will probably pay higher bills than average, while those associated with water utilities already meeting the standard should not incur new costs. Finally, EPA calculated the benefits of saving one life from cancer. The agency then offset the arsenic treatment costs by the number of lives saved (i.e., cancers avoided) and calculated a benefit-cost ratio (Table 2).
|
|
||||
|
|
||||
| Arsenic Level (ppb) |
|
|
|
|
| Total Combined Cancer Cases Avoided |
|
|
|
|
| Total National Costs ($ millions) |
|
|
|
|
| Total Combined Cancer Health Benefits ($ millions) |
|
|
|
|
| Benefits to Cost Ratio |
|
|
|
|
| Annual Cost Per Cancer Case Avoided ($ millions) |
|
|
|
|
The estimated total annual cost of implementing the 10 ppb MCL ranged from $180-205 million (Table 2). On the other hand, EPA's modeling showed nineteen to thirty-six lives saved at an annual savings of $3.7-5.5 million per cancer case. The benefit-cost ratio was estimated to be about 1, a break-even proposition. To reduce the standard any further below 10 ppb would provide an extra margin of safety, but the costs would then exceed the benefits, making any new regulation much less acceptable to cost-conscious legislators. No sense in rocking the boat too much when nearly 95% of community water supplies are already in compliance with the 10 ppb MCL.
In the end, politics rather than science are likely to determine the final MCL for arsenic. Numerous advocates will claim that scientific evidence dictates the standard be lowered to 10 ppb. Yet the chances of not getting cancer from water tainted with 10 or with 50 ppb of arsenic are hardly different. The real story, missed by the organizations supposed to inform the public, is that someone has to choose a mathematical model to estimate cancer risks, and that model is likely to be consistent with the chooser's preconceived notion of what happens at low doses. The outcome is a virtual reality, creating estimates of hazard where no data have gone before.
Dr. Allan Felsot is an Enviromental Toxicologist with WSU's Food and Environmental Quality Laboratory. He can be reached at (509) 372-7365 or by e-mail at afelsot@tricity.wsu.edu.
The Food Quality Protection Act (FQPA) of 1996 changed the landscape of food safety and pesticide use. We are now in year five of the FQPA era. Revised risk assessments of pesticides-for better or worse-are being ground through the regulatory system. In many cases, pesticide uses are being curtailed or dramatically restricted. As the U.S. Environmental Protection Agency restricts the use of key pesticides, registration of alternative products becomes even more important.
The Interregional Research Project Number 4 (IR-4) was established in 1963 to increase the availability of crop protection chemistries for minor crop producers. IR-4 is a federal/state/private cooperative that aspires to obtain clearances for pest control chemistries on minor crops. (For a complete description of IR-4's workings see "IR-4: Developing and Delivering Pest Management Solutions for Minor Crop Producers," AENews No. 162, Oct. 1999, or log onto the IR-4 national website at http://pestdata.ncsu.edu/ir-4/).
Each year, dozens of new projects are undertaken by IR-4. The new herbicide and insecticide projects initiated in 2001 are shown in the tables at the end of this article. (Fungicides will be listed in the August issue of AENews.) Remember that crop registrations listed in this table may not apply to Washington State; please consult the label. Past IR-4 projects, many of which are still in progress, can be found through the following previous link within this AENews website (http://www2.tricity.wsu.edu/aenews/April00AENews/NewProducts.html).
Each year, IR-4 receives a far greater number of requests than the program can pursue, so projects are prioritized, and only the higher-priority projects are guaranteed investigation. The prioritization process takes place at an annual meeting. The IR-4 prioritization workshop for year 2002 projects will take place in Colorado, September 11 through 13, 2001.
As the Washington State Liaison to the IR-4 program and as a Commissioner on the Washington State Commission on Pesticide Registration, I need to know the pest control needs and concerns among the diverse agricultural producers of Washington State.
The first step toward making a pesticide need known is to submit a Pesticide Clearance Request form (PCR) to IR-4. Anyone can submit a PCR; parties in Washington State can obtain them from me. I can assist interested parties in prompt submission of the form and I can help bring those needs to the attention of IR-4 at the September meeting.
Individuals or groups wishing to initiate review of a particular crop-chemistry combination should contact me right away. Washington State has a strong reputation for being proactive in pest control efforts. This is facilitated through communication between agricultural producers and university specialists. Please make your pest control needs and concerns known to me so that I can make your voice heard in Colorado.
Dr. Douglas B. Walsh is the Washington State Liaison Representative for IR-4. His office is located at WSU's IAREC facility in Prosser. He can be reached at dwalsh@tricity.wsu.edu or (509) 786-2226.
| Herbicide | Trade Name | Crop/ Registration | Registrant | Category | Comments |
| alpha- metolachlor | Dual Magnum | Registered on corn, beans, peas, potato, sorghum, onion, cabbage, and peach. Pending on tomato, grass seed, sugar beet, carrot, spinach, rhubarb, and asparagus. Potential use on garden beets, turnip greens, green onion, broccoli, melons, caneberry, blueberry, and pumpkin. | Syngenta | chloracetanilide | Same spectrum as metolachlor. |
| amicarbazone | Bay MKH | Pending registration on corn and sugarcane. | Bayer | trazolinone | Applied to the soil preplant or pre-emergence. It also has burndown activity. Soil and burndown activity are primarily on broadleaf weed species. |
| azafenidin | Milestone | Pending registration on various fruit and nut crops. | DuPont | pyridione (PPO inhibitor) | Broad spectrum pre-emergence residual herbicide. |
| BAS 615 H | Registered on small grains. | BASF | Particularly active post-emergence on Galium aparine, among other broadleaf species, in small grains. | ||
| beflubutamid | UBH-820 | Potential use on wheat, barley, rye, and triticale. | UBE Industries | phenoxy-butanamide | Post-emergence control of broadleaf weeds. |
| bensulfuron methyl | Londax | Registered on rice. | DuPont | Most broadleaf and sedge weeds. | |
| bispyribac sodium | Regiment | Pending registration on rice. | Valent | sulfonylurea (ALS inhibitor) | Annual and perennial grasses and broadleaf weeds including large and/or herbicide-resistant barnyardgrass. |
| carfentrazone- ethyl | Affinity, Aim | Registered on field corn and wheat. Pending use on sorghum, potato, barley, sweet corn, and oats. Potential use on caneberry. | FMC | aryl triazolinone | Numerous broadleaf weeds, including cocklebur and water hemp. |
| cinidon-ethyl | Lotus | Registered on barley, wheat, and oats. | BASF | isoindoldine (protox inhibitor) | Post-emergence control for broadleaf weeds. |
| clefoxydim | Aura, Tetris | Registered on rice. | BASF | cyclohexanone (ACCase inhibitor) | Controls grass weeds. |
| clethodim | Select, Prism | Registered on a wide variety of fruit, vegetable, and nut crops. | Valent | cyclohexanone (ACCase inhibitor) | Strictly a grass herbicide. |
| Collectotrichum gloeosporioides | Mallet WP | Encore Tech. | biopesticide | Naturally occuring fungus that is pathogenic to round-leaved mallow, small flowered mallow, common mallow, and velvetleaf. | |
| Herbicide | Trade Name | Crop/ Registration | Registrant | Category | Comments |
| clodinafop- propargyl | Discover | Pending registration on wheat. | Syngenta | pyridylory-phenoxy propionate | Selective post-emergence control of wild oats, annual grasses, and other weeds. |
| cloransulam- methyl | Firstrate | Registered on soybean. | Dow AgroSciences | sulfonamide (ALS inhibitor) | Pre-emergence or post-emergence control of broadleaf annual weeds. |
| cyhalofop- butyl | Clincher | Registered on barley, oats, rice, and wheat. | Dow AgroSciences | phenoxy-propionate | Post-emergence graminicide. Reduced risk pesticide. |
| diclosulam | Strongarm | Registered on peanut and soybean. | Dow AgroSciences | sulfonamide (ALS inhibitor) | Can be applied pre- or post-emergence for broadleaf weeds such as morningglory, cocklebur, velvetleaf, and nutsedge. |
| diflufenzopyr | Distinct | Registered on field and sweet corn and pasture grass. | BASF | pyridine (auxin transport inhibitor) | Controls annual grasses and broadleaf weeds. Sold in a pre-mix with dicamba. |
| dimethenamid | Frontier | Registered on dry beans, field corn, popcorn, seed corn, and grain sorghum. Pending use on dry bulb onion and garden beets. | BASF | chloroamide | Annual grasses, broadleaf weeds, yellow nutsedge control. |
| dimethenamid-P | Frontier X-2 | Pending use on corn, potato, seed grass, onion, peanut, and soybean. | BASF | chloroamide | Annual grasses, broadleaf weeds, yellow nutsedge control. |
| Drechslera monoceras | MTB-951 | Registered for use on rice. | Mitsui Chemical | biopesticide carbohydrate | |
| flazasilfuron | Mission | Registered on grape and olive. | Syngenta & ISK | sulfonylurea | Active against many grasses and broadleaf weeds with pre- and post-emergence activity. |
| florasulam | DE-570 | Unknown status on wheat, barley, and oats. | Dow AgroSciences | triazolo-pyrimidine sulfonanilide | Provides post-emergence of broadleaf weeds, particularly Galium aparine. |
| fluazolate | JV 485 | Unknown status on wheat. | Bayer and Monsanto | Pre-emergence control of broadleaf weeds and grasses. | |
| flucarbazone-sodium | Everest 70 WG | Pending use on wheat. | Bayer | sulfonyl-aminocarbonyl- triazolinones | Manages wild oat and green foxtail and certain broadleaf weeds |
| flufenacet | Axiom | Registered on corn, grass seed, potato, tomato, wheat, pepper, soybean, and onion. | Bayer | thiadizole or oxyacetamide | Soil applied for annual grasses and some broadleaf weeds. |
| flufenpyr- ethyl | S-3153 | Pending registrations on corn. Potential use on snap bean, lima bean, and dry bean. | Valent | PPO inhibitor | Excellent control of velvetleaf and morningglories. |
| flumesulam | Broadstrike | Registered on corn. Pending registration on dry bean. | Dow AgroSciences | sulfonamide (ALS inhibitor) | |
| flumiclorac | Resource | Registered for use on corn and soybean. | Valent | N-phenyl-phthalimide derivative | Post-emergence control of velvetleaf. |
| flumioxazin | Valor 50 WD | Potential use on pome fruit, stone fruit, grape, carrot, and tomato. | Valent | N-phenyl-phthalimide derivative | Controls pre-emergence broadleaf weeds with contact activity and residual soil activity. |
| fluroxypyr | Starane F | Registered on a wide variety of fruit and vegetable crops. | Dow AgroSciences | picolinic acid | Post-emergence control of annual and perennial broadleaf weeds including volunteer potato, kochia, and nightshade. |
| flurtamone | Unknown status on wheat, barley, oats, and peas. | Aventis | Pre- and early post-emergence control of annual broadleaf weeds and some grasses. | ||
| fluthiacet | Action | Currently registered on soybean. Pending registration on corn and cotton. | Syngenta | protox inhibitor | Post-emergence control for velvetleaf, lambsquarter, and other broadleaf weeds. Also desiccant use. |
| foramsulfuron | AE F130360 | Pending registration on corn and sugarcane. | Aventis | sulfonylurea (ALS inhibitor) | Post-emergence control of most annual and perennial grasses. |
| glufosinate | Liberty, Rely | Registered on apple, grape, potato, and field corn. Pending use on sweet corn, canola, and sugar beet. | Aventis | Broad spectrum, non-selective. | |
| glyphosate | Roundup | Registered on a wide variety of commodities. | Monsanto/ Gowan | isopropylamine salt | Controls grasses and broadleaf weeds. |
| halosulfuron | Permit | Registered on field and sweet corn and grain sorghum. Pending use on cucurbits. Potential use on snap/dry beans, asparagus, and potato. | Monsanto/ Gowan | sulfonylurea | Controls nutsedge, velvetleaf, cocklebur, and other broadleaf weeds. |
| imazamox | Raptor | Pending use on edible legumes and canola. | American Cyanamid | imidazolinone | Pre- and post-emergence control of annual grasses and broadleaf weeds. |
| isoxaflutole | Balance | Registered on field corn. Pending use on sweet corn, wheat, and barley. | Aventis | isoxazole | Soil applied for many annual grasses and some broadleaf weeds. |
| Herbicide | Trade Name | Crop/ Registration | Registrant | Category | Comments |
| mesotrione | Pending use on field corn. Potential use on sweet corn. | Syngenta | cyclohezanedione | Pre- and post- emergence management of annual grasses and broadleaf weeds, including sulfonylurea-resistant weeds. | |
| oxadiargyl | Topstar 80 WP | Potential use on vegetables and tree crops. | Aventis | oxadiazol | Broad-spectrum weed control, similar to oxidiazinon. |
| oxasulfuron | Dynam, Expert | Pending registration for use on soybean. | Syngenta | sulfonylurea (ALS inhibitor) | Post emergence use for cocklebur, ragweed, and other broadleaf weeds. |
| pelargonic acid | Registered on all crops. | Dow AgroSciences | biopesticide | Contact, non-selective. | |
| picolinafen | AC 00001 | Pending registration for use on barley, rye, triticale, and wheat. | BASF | Aryloxpicolinamide (inhibits phytoene desaturase) | Post-emergence control of annual broadleaf weeds. |
| prosulfuron | Peak | Registered on various cereal crops. Pending registration on sugarcane. | sulfonylurea (ALS inhibitor) | Post-emergence control of cocklebur, kochia, lambsquarter, pigweed, ragweed, and velvetleaf. | |
| propoxycarbazone | Olympus, Attribute | Pending registration for use on rye, triticale, and wheat. | Bayer | sulfonylaminocarbonyl trizolinone (ALS Inhibitor) | Post-emergence grass weed control and broadleaf weed control in the Cruciferae family. |
| pyraflufen-ethyl | Ecopart | Pending use on wheat and potato. | Nihon Nohyaku | protox inhibitor | Post-emergence herbicide for general non-selective control of weeds or use as dessicant. |
| pyribenzoxim | Pyanchor | Pending registration for use on rice. | Rohm & Haas | Post-emergence material with broad-spectrum activity on annual and perennial weeds including grasses, broadleaves, and sedges. | |
| pyridate | Tough | Registered on various row crops. Pending registration on alfalfa. | Syngenta | phenylpyridazine | Controls broadleaf weeds. |
| pyrithiobac- sodium | Staple | Registered for use on cotton. | DuPont | pyrimidinyl carboxy | Pre- and post-emergence control of a wide range of broadleaf weeds. |
| quinclorac | Facet, Paramount | Registered for use on rice, sorghum, and wheat. | BASF | quinoline carboxylic acid | Post-emergence control of annual grasses and certain broadleaf weeds. |
| quizalofop- ethyl | Assure | Registered and pending registration on a wide variety of crops. | DuPont | phenoxy proprionic ester | Post-emergence grass herbicide |
| rimsulfuron | Matrix | Registered on field corn, potato, and tomato. | DuPont | sulfonylurea (ALS inhibitor) | Annual grass and broadleaf weed control. |
| sethoxydim | Poast | Registered on a wide variety of crops. | BASF | cyclohexanedione (ACCase inhibitor) | Post-emergence herbicide. |
| sulfentrazone | Authority | Registered on grain and row crops. | FMC | aryl trazolinone | Controls broadleaf and grass species. |
| sulfosulfuron | Maverick | Registered on a variety of grain crops. | Monsanto/ Gowan | sulfonylurea (ALS inhibitor) | Controls grasses/broadleaf weeds including quackgrass, bromes, and mustards. |
| tepraloxydim | Equinox, Aramo | Pending registration on sugar beet, cotton, leek, onion, and soybean. | BASF | cyclohexandione (ACCase inhibitor) | Provides post-emergence grass weed control in broadleaf crops, at lower rates. At higher rates, it will control perennials such as johnsongrass and will suppress Bermuda grass. |
| thiazopyr | Visor | Currently registered on several crops. Pending registration on a wide variety of fruit crops. | Rohm & Haas | pyridine | Controls annual and broadleaf weeds, including crabgrass and |
