Central Chemical Corp.

History of Central Chemical Corp.
In important ways, the circumstances surrounding Thomas’s entry into the fertilizer business were not propitious. First, Thomas began business near the end of a half-century-long relocation of the fertilizer industry’s center. Though fertilizer use continued to increase in the Mid-Atlantic states and elsewhere during the period from 1870 to 1920, the manufacture of fertilizer began to shift to the Southern states in the late nineteenth century. By 1902, Charleston had replaced Baltimore as the fertilizer capital of the country. The Mid-Atlantic states’ share of total fertilizer use decreased from 34% in 1880 to 14% in 1920. By contrast, in 1920 the South-Atlantic states used about 50% of all fertilizers consumed in the U.S. Thus, Hagerstown could no longer enjoy proximity to the major centers of fertilizer-material production, and, while previously situated between the two highest-fertilizer-use regions of the country, it now found itself on the northern edge of a region that now dwarfed all others.

Second, Thomas’s decision to continue in the practice (apparently favored by Hagerstown companies) of making fertilizer primarily from bone and organic materials came at the start of a rapid increase in the demand for mixed fertilizers, but also at the beginning of a precipitous decline in the use of bone and bone products as a source of phosphorous in fertilizers. With the growing use of potash and phosphate rock, consumption of mixed fertilizers grew from 46% of the total in 1880 to around 70% in 1920. During the period from 1890 to 1910, when Thomas was focusing on his presumably unmixed “dissolved bone” fertilizers, mixed fertilizers were capturing market share.

Furthermore, the period from 1880 to 1920 is also characterized by the decreasing use of organic materials in general. Though organic materials provided about 91% of the total nitrogen in 1900, by 1917 the total nitrogen contribution from organics had dropped to 46.5%. With regard to phosphates, bone meal, dissolved bones and boneblack, and phosphoro-guano use peaked in 1890, but their use dropped to a negligible amount by 1910 as the use of superphosphates from phosphate rock increased dramatically..

Third, even as Thomas had begun his business trading fertilizer for livestock from relatively distant places, the fertilizer industry was increasingly turning to local distribution. Though mid-nineteenth-century fertilizer plants typically were situated in East Coast harbor cities, twentieth-century plants were dispersed to be closer to areas of consumption.

Finally, even though the name “Thomas’ Dissolved Bone” suggests that Thomas produced his own superphosphates initially, the use of bone in the production of superphosphates was on its way out as described above. For all practical purposes, then, Thomas had set his business on the track of the second, smaller type of fertilizer company, which only mixed fertilizer and did not produce superphosphates. For the next 90 years, even when Central Chemical had affiliates across the nation, it would remain in this “smaller” category – relying on large suppliers for its materials. For reasons noted above, this was not a problem at the turn of the century vis-à-vis the larger companies. Starting in the 1890s, however, many agricultural societies began to advocate home mixing of fertilizer materials by farmers. Throughout the first half of the twentieth century, the fertilizer industry fought this effort successfully by insisting on the value of industrial mixing processes and the farmer’s comparative disadvantages in mixing.

Though in its early years, Central Chemical advertised itself as “Exporters – Manufacturers – Importers,” by the 1970s it had become little more than a middle-man between larger suppliers and farmers. It did not import its own materials, but purchased granulated materials from suppliers. There is no evidence that Central Chemical was exporting products out of the country anymore. And its manufacturing capacity consisted of mixing pre-processed granulated materials in various proportions. At this point, its consulting capacity became equally important to its factory processes.

Though Central Chemical and its subsidiaries were taking in a combined $25 million in sales by the late 1970s, an employee remembers that there was always a sense of trouble on the horizon. The vulnerability of a company that adds very little value to its product and relies entirely on contracts with larger suppliers requires no explanation. It appears that not long after Central Chemical became a bulk blender, its large suppliers began pushing their advantages. In the early 70s, Central Chemical’s supplier, Agrico Chemical Company, put pressure on Central Chemical to enter into a long-term contract. When Central Chemical refused, Agrico withheld di-ammonium phosphate and granular triple super phosphate at a time of national shortage in these materials. Central Chemical responded by filing an antitrust lawsuit against Agrico in federal court. For most of the next decade much of the time, resources, and energy of what was still a closely-held corporation would be consumed in this litigation. Ultimately the lawsuit proved unsuccessful.

All of this came at the same time that local, state, federal regulators were investigating the Hagerstown plant for its pesticide-disposal practices. In the 1970s the State of Maryland ordered two separate cleanups of the site; the EPA was just getting started.

Ultimately the push to eliminate the middle man that drove the switch to bulk blending began to turn on the blenders themselves. The larger companies and farmers wised up, and realized that they could both save money by dealing directly with each other. Farmers began buying direct-application materials from the same suppliers used by Central Chemical. By the early 1980s, Central Chemical’s network of fertilizer blenders had contracted substantially. Blending operations like those of the Hagerstown plant could no longer make the case for themselves. Crushed under the weight of increasingly serious environmental liability for its mid-century disposal practices, the Central Chemical Corporation contracted its operations substantially. The Hagerstown plant ceased operations in 1984 and the office headquarters moved from the old Thomas building to an office outside Hagerstown.


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Wednesday, June 24, 2015

IARC Monographs evaluate DDT, lindane, and 2,4-D


Published: 
The International Agency for Research on Cancer (IARC), the specialized cancer agency of the World Health Organization, has evaluated the carcinogenicity of the insecticides gamma-hexachlorocyclohexane (lindane) and dichlorodiphenyltrichloroethane (DDT) and the herbicide 2,4-dichlorophenoxyacetic acid (2,4-D).

After thoroughly reviewing the latest available scientific literature, a Working Group of 26 experts from 13 countries convened by the IARC Monographs Programme classified the insecticide lindane as carcinogenic to humans (Group 1). There was sufficient evidence in humans for the carcinogenicity of lindane for non-Hodgkin lymphoma (NHL).

The insecticide DDT was classified as probably carcinogenic to humans (Group 2A), based on sufficient evidence that DTT causes cancer in experimental animals and limited evidence of its carcinogenicity in humans. Epidemiological studies found positive associations between exposure to DDT and NHL, testicular cancer, and liver cancer. There was also strong experimental evidence that DDT can suppress the immune system and disrupt sex hormones. However, overall there was no association between breast cancer and DDT levels measured in samples of blood or fat.

The herbicide 2,4-D was classified as possibly carcinogenic to humans (Group 2B), based on inadequate evidence in humans and limited evidence in experimental animals. There is strong evidence that 2,4-D induces oxidative stress, a mechanism that can operate in humans, and moderate evidence that 2,4-D causes immunosuppression, based on in vivo and in vitro studies. However, epidemiological studies did not find strong or consistent increases in risk of NHL or other cancers in relation to 2,4-D exposure.
A summary of the final evaluations is available online in The Lancet Oncology, and the detailed assessments will be published as Volume 113 of the IARC Monographs.

Lindane has been used extensively for insect control, including in agriculture and for treatment of human lice and scabies. High exposures have occurred among agricultural workers and pesticide applicators; however, the use of lindane is now banned or restricted in most countries. Large epidemiological studies of agricultural exposures in the USA and Canada showed a 60% increased risk of NHL in those exposed to lindane.

DDT was introduced for the control of insect-borne diseases during the Second World War and was later applied widely to eradicate malaria and in agriculture. Although most uses of DDT were banned from the 1970s, DDT and its breakdown products are highly persistent and can be found in the environment and in animal and human tissues throughout the world. Exposure to DDT still occurs, mainly through diet. The remaining and essential use of DDT is for disease vector control, mainly for malaria. This use is strictly restricted under the Stockholm Convention.


Since its introduction in 1945, 2,4-D has been widely used to control weeds in agriculture, forestry, and urban and residential settings. Occupational exposures to 2,4-D can occur during manufacturing and application, and the general population can be exposed through food, water, dust, or residential application, and during spraying.

http://www.medicalnewstoday.com/releases/295836.php?tw
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Monday, June 8, 2015

Parkinson's Disease and Pesticides: What's the Connection?

Scientists find a way chemicals may contribute to Parkinson’s

By Bret Stetka | April 8, 2014



The pesticide Parkinson's connection

Thinkstock
What exactly causes Parkinson’s disease is far from figured out. But a clue has been lurking in cornfields for years.

The data confirm it: farmers are more prone to Parkinson’s than the general population. And pesticides could be to blame. Over a decade of evidence shows a clear association between pesticide exposure and a higher risk for the second most common neurodegenerative disease, after Alzheimer's. A new study published in Neurology proposes a potential mechanism by which at least some pesticides might contribute to Parkinson’s.

Regardless of inciting factors — and there appear to be many — Parkinson’s ultimately claims dopamine-releasing neurons in a small, central arc of brain called the “substantia nigra pars compacta.” The nigra normally supplies dopamine to the neighboring striatum to help coordinate movement. Through a series of complex connections, striatal signals then find their way to the motor cortex and voila, we move. But when nigral neurons die, motor function goes haywire and the classic symptoms set in, including namely tremors, slowed movements, and rigidity.

Pesticides first came under suspicion as potentially lethal to the nigra in the early 1980s following a tragic designer drug debacle straight out of Breaking Bad. Patients started showing up at Northern California ERs nearly unresponsive, rigid, and tremoring — in other words, severely Parkinsonian. Savvy detective work by neurologist Dr. William Langston and his colleagues, along with the Santa Clara County police, traced the mysterious outbreak to a rogue chemist and a bad batch. He’d been trying to synthesize a “synthetic heroin” — not the snow cone flavorings he claimed — however a powder sample from his garage lab contained traces of an impurity called MPTP. MPTP, it turned out, ravages dopaminergic neurons in the nigra and causes what looks like advanced Parkinson’s. All of the newly Parkinsonian patients were heroin users who had injected the tainted product. And MPTP, it also turned out, is awfully similar in structure to the widely used herbicide paraquat, leading some neurologists to turn their attention to farms and fields.

In 2000, a meta-analysis linked confirmed and presumed pesticide exposure with increased risk of Parkinson’s. Subsequent work supported this connection, including a large 2006 study that followed patients for nine years. The patients exposed to pesticides had a 70% higher incidence of Parkinson’s when the study ended; the risk was the same for exposed farmers and exposed non-farmers, hence some other farm-related factor wasn’t to blame. The study didn’t report on specific toxins, but more recent work out of The Parkinson’s Institute in Sunnyvale, CA, founded by Langston after the MPTP discovery, did. The authors took detailed occupational and exposure histories from farmers and their families. Paraquat upped Parkinson’s risk 2.5-fold. Rotenone was also red-flagged.

Pesticides exert their neurotoxicity in a number of ways. Both paraquat and rotenone appear to wither dopaminergic neurons via free radical production. Free radicals are atoms or molecules with an unpaired electron looking for a partner; they do major cellular damage by pilfering electrons from other molecules, impairing their function. Rotenone may also interfere with the normal neuronal clearance of damaged or degraded proteins. Faulty proteins accumulate, derailing various cellular processes.

The new study, from a team at UCLA, proposes yet another mechanism by which some pesticides might contribute to Parkinson’s. It might also provide a major lead in understanding the disease. The team had previously found that the fungicide benomyl was associated with increased Parkinson’s risk and damaged the brain by inhibiting an enzyme called ALDH that normally helps metabolize fats, proteins and toxins like alcohol (certain ALDH mutation carriers have to take it easy at the bar). ALDH also detoxifies the dopamine metabolite DOPAL. When the enzyme isn’t working properly, DOPAL builds up in neurons and may explain the loss of dopaminergic neurons in Parkinson’s. This time around the authors tested 26 pesticides, first for their influence on ALDH activity in rat neurons and next for any epidemiologic association with Parkinson’s. Eleven pesticides inhibited ALDH at the concentration tested, eight of which could be included in the study based on available histories from 360 rural Californian patients. All eight were associated with an increased Parkinson’s risk and genetic variation in the ALDH2 subtype of the enzyme increased the risk further in those exposed. The findings not only point to new culprit compounds, but reflect the growing appreciation of Parkinson’s as a multifactorial disease, in many cases due to the collusion of both genetic and environmental factors.

At least 10% of Parkinson’cases are now thought to be due primarily to specific gene variants, and estimates suggest that genetics may contribute to upwards of 20% to 50%. Patients with a few specific mutations — common in people of Mediterranean descent — carry a nearly 100% chance of developing the disease. Though, as lead author Dr. Jeff M. Brontstein commented to Scientific American, while a minority of cases might be primarily due to a specific genetic or environmental risk factor, ultimately many if not most cases are likely due to gene-environment interactions. This may explain why there isn’t an epidemic of Parkinson’s in rural areas. Despite the large number of people regularly exposed to pesticides, not everyone has a genetic susceptibility.

This gets incredibly complicated when you consider the possibility of multiple genetic and environmental risk factors working together. It's clear that pesticides wreak havoc on the brain through a variety of mechanisms. Hence farmers and others regularly exposed are at risk for a multipronged, possibly cumulative attack. Certain industrial solvents also appear to bump up Parkinson’s vulnerability. Head trauma, in combination with a particular mutation, does too. And diets high in omega-3 fatty acids, found in fish, plant and seed oils, appear to protect against the disease. The laundry list of risk factors and contributors could explain the varied symptoms experienced by Parkinson’s patients. Some present early in life, some late. For many the classic motor symptoms predominate; others present with non-motor findings like sleep disturbances, constipation and depression. No two cases are identical.

The confusion isn’t just clinical. Recent evidence positions Parkinson’s as one of a number of related neurodegenerative disorders marked by the accumulation of abnormal proteins in the brain, including Alzheimer’s disease and ALS. They all appear partially genetic, partially environmental and probably in many cases both. Neuronal protein accumulations called Lewy bodies — a pathologic hallmark of Parkinson’s — are also found in the brains of Alzheimer’s patients; PD-afflicted brains often contain the amyloid protein aggregates common to Alzheimer’s. It’s a Venn diagram of neurodegeneration.

The new findings further confirm that those whose livelihood relies on repelling pests should pay mind to their increased risk for Parkinson’s, particularly if they have other known risk factors, and take precautions. They can limit exposure and avoid the riskier compounds. They can wear masks, clean up spills and wash up vigorously. Moreover, implicating ALDH in Parkinson’s pathology could represent an important step toward determining a final common pathway on which the various risk factors converge, a potential holy grail for drug development, and ultimately for patients. Rarely are neurologic diseases straight forward, and Parkinson’s has proved no different. But a terribly unfortunate outcome for many in search of heartier, healthier crops may have brought medicine one notch closer to deciphering a frustratingly complex disease.


http://www.scientificamerican.com/article/parkinsons-disease-and-pesticides-whats-the-connection/

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