In Washington DC, a coalition of consumer and environmental pressure
groups are fighting to have the GATT either rewritten or buried. They say
the draft agreement could undermine American laws governing pesticides,
nutritional labelling of food products, cancer-causing chemicals in food
and several environmental laws.

Environmentalists have always been sceptical of the intentions behind
the GATT (‘Trade deals a blow to the environment’, ¿ìè¶ÌÊÓƵ, 10 November
1990). The latest draft is, if anything, worse than earlier ones, they say.
So the coalition has intensified its opposition.

Public Citizen, a Washington consumer group, has filed a suit to force
the US to draw up a statement on the environmental impact of the GATT agreement.
Backing it are members of Congress who say the deal will be rejected if
it undercuts national law.

‘The latest draft is in no way an environmental document,’ says John
Audley of the Sierra Club, an environmental pressure group. ‘It just encourages
trade.’ American trade officials reply that the government will support
the draft anyway ‘and they show no sign of giving in’, says Audley.

Nor has the GATT draft linked the words ‘sustainable’ and ‘development’,
as environmentalists had hoped, says Charles Arden-Clarke of World Wildlife
Fund international in Geneva. The new GATT could undermine efforts by developing
countries to control exports of nonrenewable resources such as hardwood
trees, he warns.

Indonesia, for example, banned the export of logs on environmental
gounds. The European Community challenged the ban under GATT rules, arguing
that Indonesia was trying to monopolise manufacture of such goods as furniture
because it could earn more by selling manufactured goods than from raw timber.

Within the GATT itself, such arguments are taken very seriously, says
Arthur Dunkel, the director-general of the GATT. ‘The danger of a proliferation
of different national environmental standards leading to trade policy friction
is very real,’ he told a conference in Bangkok last week. ‘The problems
involved are not only highly complex but also politically delicate.’

In the US, environmentalists have homed in on several portions of the
final draft of the Uruguay round talks. For example, the GATT would ‘harmonise’
international ‘sanitary and phytosanitary standards’. These govern such
things as pesticide residues on food in international trade. If a country’s
standards on residues are stricter than the international standard, they
could be challenged as a barrier to trade.

The proposed ‘harmonised’ standard is set by the Codex Alimentarius
Commission, the body charged with setting food standards by the WHO and
the Food and Agricultural Organization. According to Public Citizen, many
Codex standards on pesticides are less strict than American standards. Codex,
for example, would permit 50 times as much DDT on peaches, 33 times as much
on broccoli, and 10 times as much on apples than the US allows, says the
group.

The US government requires processed food to carry labels listing the
amount of salt, fat and other ingredients. Another regulation, known as
the Delaney clause, bars the inclusion in processed food of any substance
that causes cancer in laboratory animals. All could fall foul of the GATT,
say critics. So could laws passed by states that have tougher limits than
the US government’s. California, for example, has stricter limits on pesticides
in food and water than the federal government requires.

Public Citizen and its coalition partners argue that the GATT’s attempts
to lower ‘technical barriers to trade’ allow foreign governments to break
American laws. They also argue that the US government should be allowed
to project its environmental laws beyond its own borders. For example, California
has a law barring any pesticide residues on food. If this ban is challenged
under the GATT rules, California would have to prove that its law rests
on ‘strong scientific principles’ before a panel of international experts.
‘They are usually trade specialists, not scientists, and they meet in secret,’
says Audley.

Last year, argument over conflicting American laws and GATT regulations
erupted into an international row. The US banned imports of Mexican tuna
because Mexican tuna boats also catch dolphins in their nets. Last August,
a GATT panel overturned the ban, saying the US could not extend protection
of the health of plants, animals or humans beyond its borders. Nor could
it sanction products based on the ‘process’ by which they are made. In the
case of tuna, it was not the fish that the US objected to but the way they
were caught. The latest draft of the agreement codifies the panel’s decision
and extends it to all signatories to the agreement.

Even some environmental activists view the US objection on this point
as protectionism. Yet the draft agreement may hinder international pacts
covering the ‘global commons’. The Montreal Protocol for protecting the
ozone layer, for example, relies on trade sanctions for enforcement. ‘GATT
does not help solve the ‘free rider’ problem,’ in which countries such as
China benefit from a safer environment without abiding by the protocol,
says Arden-Clarke.

The environmental critics also argue that US laws protecting endangered
species, such as the African elephant set sanctions according to how the
product, ivory for instance, is taken. As with tuna, this too could be challenged
under the GATT rules.

Enforcement of the agreement is expected to be taken over by a new ‘multilateral
trading organisation’ (MTO). Permanent and independent, the MTO would have
broad legal powers to enforce GATT decisions within member countries. The
MTO would be bigger than the expert panel that now handles disputes under
GATT rules.

There is particular repugnance towards the MTO in the US Congress. Developing
countries are also wary of the MTO’s power to permit cross-retaliation’.
If, for example, Brazil denied US companies access to its telecommunications
market, the US could respond by blocking imports of Brazilian timber. ‘MTO
is a bigger bully with a bigger stick,’ says Arden-Clarke.

Too much cholesterol in the blood can line arteries with plaque, causing
atherosclerosis, or hardening of the arteries. Diet, exercise and smoking
influence the fate of cholesterol, but so do several genes. Last week, scientists
in Texas said they had cracked the code for one such gene, and their results
could help in predicting who is at risk.

The gene is one of several that produce apolipoproteins, components
of the lipoproteins that shuttle cholesterol through the bloodstream and
to the liver. Called APOe, the gene comes in several versions, or alleles.
The three most common are called E2, E3 and E4.

Everyone has two versions of the gene, one inherited from each parent.
Fifty-seven per cent of the population is E3/E3, 24 per cent is E3/E4, and
13 per cent is E2/E3; other combinations are rare.

James Hixson, a geneticist at the Southwest Foundation for Biomedical
Research in San Antonio, Texas, examined DNA from 683 men, aged between
15 and 34, who had died in accidents. He then compared the allele type with
maps of the walls of major arteries removed during autopsy.

Every subject had some plaque covering the interior walls of their abdominal
artery. But those with the genetic combination E3/E4 showed the most damage;
32 per cent of the artery was covered. Those with the combination E3/E3
were somewhat better off, with 29 per cent covered, while the E2/E3 group
had 23 per cent damage.

The differences may seem small, says Hixson, but they are statistically
significant considering how young the subjects were. ‘The differences in
damage are expected to widen over time,’ he says. The subjects with the
E2/E3 allele had almost 40 per cent less damage than the E3/E4 group, suggesting
that the E2 allele has a positive effect on clearing cholesterol from the
bloodstream.

Other studies have linked the E4 allele to a higher risk of heart attack.
In addition, Hixson found that the E2 allele is associated with lower blood
levels of low-density lipoprotein, believed to be the more harmful form
of cholesterol. ‘All this is really consistent,’ Hixson says, ‘which is
why I’ve started thinking about genetic testing. I think in 10 years or
so it’s going to be part of predicting health.’

Screening young people for a genetic predisposition to atherosclerosis
would pinpoint those who especially need to watch their diet and behaviour,
says Virgil Brown of the American Heart Association. Some 20 genes have
already been implicated in the body’s cholesterol pathway, but Frederick
Cornhill of Ohio State University, says Hixson’s research is the first to
show that a single gene is probably as important as any of the traditional
behavioural causes of the disease.

Britain approved an engineered yeast for making bread last year. The
US followed with chymosin, a milk-clotting enzyme made by genetically engineered
bacteria. Some 35 per cent of American cheese is now made with the commercial
version, called Chymax. More foods will soon be intro duced, such as oils
that are low in unsaturated fat, fish that grow fast on mammalian hormones
and plants with built-in pesticides.

But these products may remain on the shelf if the Environmental Defense
Fund (EDF) has its way. The pressure group has petitioned the government
to apply its rules for chemical additives to any food that has been altered
by genes made in the laboratory.

The Food and Drug Administration (FDA) has no specific criteria for
judging the safety of genetically engineered food. These products may be
considered simply a new food, a food ‘generally regarded as safe’, or a
food additive. Rules for food additives, designed for chemicals such as
saccharin, demand the most extensive proof of safety from their makers.

The EDF wants all the products of altered or introduced genes – so-called
expression products – that end up in food to be considered additives. They
also want these rules to apply where the food has been changed by genetic
engineering, even if no expression products are present in the final product
– for instance, an oil which is low in fat because the plant it comes from
has been engineered to produce low-fat oil.

No one has shown that genetically altered foods are safe, says Rebecca
Goldburg of the EDF. On the other hand, no one has shown them to be unsafe,
says Alan Goldhammer of the Industrial Biotechnology Association, which
opposes the EDF’s petition.

The EDF points to the case of the nut-ritional supplement L-tryptophan,
which caused 27 deaths and 1500 cases of serious illness in 1990. L-tryptophan
was made by a genetically engineered bacterium created by a Japanese company,
Showa Denko. No evidence so far proves that the gene alteration was at fault.
But Goldburg suggests other kinds of complications that might be associated
with genetically engineered foodstuffs. A new gene in a plant could increase
the plant’s production of natural toxins. Or it could alter the nutritional
value of the food.

One new food soon to reach the shops is transgenic fish made to grow
faster with the help of mammalian growth hormones. The EDF says that transferring
genes for growth hormone from mammals into fish has ‘obvious potential to
harm humans’. Rex Dunham at Auburn University in Alabama has done exactly
this with several species of fish, and disagrees: ‘The DNA performs a very
specific function regardless of the source . . . besides, we eat mammals
with growth hormone all the time.’

The biotechnology industry is just as keen on having the rules clarified
as the EDF, otherwise there is likely to be a backlog of products waiting
for approval. But they say EDF goes too far. An industrial consortium has
offered a plan that would treat genetically engineered substances the same
way as those produced through breeding. They say that the strictest type
of regulations should be applied only to foods with altered genes which
produce substances that would be considered food additives if they were
made conventionally.

Food additives such as colourings and sweeteners can take years to approve,
says James Maryanski of the FDA. New foods, on the other hand, may go directly
to market with little oversight.

The FDA is due to decide its new policy for genetically engineered foods
by January. Whatever it decides, responsibility for regulating new foods
is likely to be complicated. The Environmental Protection Agency, for example,
would investigate genetic changes meant to confer pest resistance to, say,
apple trees. If another genetic alteration affects how nutritious the apples
are, however, the FDA would review it.

‘Genetics is probably responsible for half of all primary hearing loss
in North America,’ says Mary-Claire King, a molecular biologist and epidemiologist
at the University of California at Berkeley. ‘Clinically this deafness is
unusual. Genetically it may turn out to be caused by alterations in the
same gene that causes many other kinds of deafness.’

King received a grant and orders last May from the National Institutes
of Health: find the genetic cause of inherited deafness in three years.
By chance, Pedro Leon, a biologist and physiologist from the University
of Costa Rica, was working in King’s laboratory at the time.

‘I had heard of this deafness in 1977,’ says Leon, who announced the
discovery at the Eighth International Congress of Human Genetics in Washington
DC. The deafness occurs only in Cartago, in north central Costa Rica. During
the 1980s, researchers at the University of Costa Rica located more than
500 people who suffered from it and traced their genealogy to a single individual,
Felix Monge. Born in 1770, Monge had been able to speak but, according to
historical documents, was profoundly deaf.

The syndrome, handed down over the generations, shows up first as a
form of low-frequency hearing loss for sounds at 125 to 150 hertz. Children
begin to lose their ability to hear these sounds in early adolescence. By
their 30s or 40s, they are completely deaf. ‘Because they lose their hearing
slowly, they become very proficient lip-readers,’ says Leon. ‘Many people
in Cartago simply mouth words to each other silently.’

With Monge, says Leon, sound is apparently transmitted normally to the
inner ear, and the auditory nerve is intact. The defect appears to be in
the apex of the cochlea, the spiral tube in the inner ear that conducts
sound to the nervous system.

On average, in a family with one deaf partner, two out of every four
children develop the disability. This means that the deaf partner is usually
heterozygous, with one normal gene and one faulty gene, but the dysfunctional
gene dominates.

Monge deafness and the Cartago community were ideal for gene hunting.
The families were large and local historical records well kept. Also, their
deafness was genetically ‘pure’: every affected person but one had married
a hearing person, so no other type of inherited deafness could confuse the
results. Nor were any other disabilities associated with Monge. ‘This situation
was unique,’ says King. ‘When you undertake a genetic analysis, the most
efficient way to solve a global problem with many possible different causes
is to go after the clearest individual example of it.’

Leon, King and their colleagues are studying some 500 people in 53
families. About 100 people are now deaf and many more will become so. The
scientific team has sampled DNA from 86 people so far. By cutting the chromosomes
with a range of enzymes, the researchers found differences between fragment
patterns in affected and unaffected relatives.

The researchers also used labelled probes, small bits of DNA from various
known parts of the 46 human chromosomes that will attach to their original
sites when mixed with DNA. Probes from chromosome 5 zeroed in on the unusual
DNA fragments from Monge individuals.

King and Leon have narrowed the Monge gene to a large section of chromosome
5. They have yet to find the gene itself but they have several markers located
near to it on the chromosome. From there, they can work in towards the gene
and then sequence its chemical structure and discover the flaw that causes
the deafness.

In the meantime, says Leon, the markers will allow them to predict which
children in these families will become deaf. The University of Costa Rica
has set up a clinic to counsel these families and prepare their children
for the onset of the deafness, which has no cure.

The Spacelab life sciences mission aboard the shuttle Columbia was dedicated
to studying biology and medicine. Seven astronauts – three women and four
men – conducted almost 40 experiments, many of which had never before been
performed on humans in space. The mission also carried 29 rats and more
than 2000 jellyfish.

The experiments turned up some surprises. ‘The results have changed
some of our thinking,’ says Arnauld Nicogossian, director of life sciences
at NASA. ‘But we are now more sure that it will be feasible and safe to
go to Mars.’

Despite Nicogossian’s claim, the biggest potential hazards to long space
missions are cosmic radiation and the possibility of life support systems
not working over years of travel. These were not addressed directly in the
flight.

Another worry scientists had was that the shift of fluids to the upper
body during weightlessness might lead to pulmonary oedema. ‘We can put that
to rest now,’ says Nicogossian. Astronauts had blood, urine and a host of
physiological profiles taken for months before and after the flight.

One finding sheds light on ‘space anaemia’, a condition in which a person’s
red blood cell count drops during space flight. It was thought that the
condition occurs as a result of the body removing more red blood cells than
usual. But experiments showed that a reduction in output of new red cells
by the bone marrow is responsible.

Carolyn Leach of the life sciences division at Johnson Space Center
in Houston, Texas, believes that this may be a reaction to the shift in
blood within the body. The body falsely ‘senses’ that it has too much blood,
she says. Leach also notes that the kidneys filter blood at a greater rate
in weightless conditions, while blood plasma flows more slowly.

An unfortunate effect of space flight is a drop in the activity of white
blood cells, which fight disease. Any such change is worrying because the
enclosed environment of a space capsule encourages the spread of disease.
Augosto Cogoli of the Swiss Federal Institute of Technology in Zurich confirmed
the effect on white blood cells during test-tube experiments aboard the
shuttle. However, he found that the activity of white cells improved if
‘microcapsules’ were added to force the cells into contact with each other.

Some findings of the mission shed light on the working of particular
organs. The astronauts’ lungs, for example, did not behave quite as expected.
In full gravity, the flow of air and fluids in the pulmonary passageways
is not uniform. ¿ìè¶ÌÊÓƵs had expected that in conditions of weightlessness
the flow would become uniform. It did not, though at present no one knows
why.

Jellyfish made their debut in space aboard the shuttle flight. According
to Laurence Young of the Massachusetts Institute of Technology, their passage
on the flight was justified by the need to study how weightlessness affects
the development of their statoliths – the organs with which they orient
themselves. Statoliths are similar to otoliths in the human ear, which are
associated with the space sickness that strikes most astronauts.

Young says the jellyfish organs grew normally, as did otoliths of the
rats aboard the shuttle. However, the rats grew more than the usual number
of the neural synapses that carry signals from the otoliths. Young believes
this is part of the animals’ adaptation to weightlessness, and that it bolsters
the idea that space sickness is caused by sensory conflict along this neural
pathway.

Last week’s guidelines from the Centers for Disease Control in Atlanta,
Georgia, say hospitals should ‘offer and encourage’ patients to take a test,
although they say patients should remain free to refuse. The CDC’s opponents
say this is a step toward mandatory testing, while others argue that it
does not go far enough.

Representative Henry Waxman of California attacked the proposal. ‘What
steps are being planned to provide health care, protect health insurance,
and get pharmaceuticals to these patients?’ he asked. Meanwhile, Representative
William Dannemeyer of California said patients should not be free to refuse
a test, claiming this would be ‘allowing the civil rights of the infected
to take precedence over the rights of the uninfected’.

Until now, the CDC has advised hospitals to encourage HIV tests only
for patients known to be at high risk of infection, such as intravenous
drug users. According to William Roper, the institution’s director, the
new approach stems from the continuing spread of the virus. Studies from
urban hospitals have found that between 0.3 and 6 per cent of patients are
infected. In two studies, it emerged that two-thirds of these patients did
not know they were infected.

Roper argues that the guidelines are not intended to protect health
workers. He says staff should take routine precautions to control the spread
of infection, such as wearing rubber gloves for some procedures. The real
purpose of the guidelines, says Roper, is to ensure that infected patients
get the proper type of care. ‘People need to know whether they are HIV-infected,’
he says. He adds that no patient would be forced to take a test.

In Britain, a spokeswoman for the Department of Health told ¿ìè¶ÌÊÓƵ
that it had not yet considered the CDC’s guidelines, but that the British
position remains unchanged. Neither health workers nor patients in Britain
are asked routinely to have a test, except patients in certain antenatal
clinics.

The British Medical Association believes it unlikely that the CDC’s
recommendations would be copied in Britain, because the prevalence of HIV
is so much lower than in the US. The Royal College of Surgeons is reviewing
its guidelines, but its present position is that routine testing would be
‘impractical and illogical’. It would also be costly, because all patients
would have to be offered counselling.

Nick Partridge, spokesman for the Terrence Higgins Trust, says the proposal
would not help health workers. He also argues that hospital is not the best
place for people who are already ill to find out they are HIV-positive.
‘People will come forward for testing when effective treatments are available
and when fear of discrimination is removed. That’s the way to encourage
testing, not to impose it on patients when they are ill,’ he says.

The risk to either patient or doctor of catching HIV during a procedure
is very low. Even when a health worker pricks his or her finger with a contaminated
needle, the risk of infection is about 1 in 300. In the US, some 24 health
workers are known to have been infected with HIV during the course of their
jobs. A handful of patients have been infected with HIV through a medical
procedure, all of them patients of the same dentist in Florida (This Week,
2 March).

The CDC recommendation came in the same week that experts descended
on Congress to defend health care workers. In July, the CDC suggested that
people who perform invasive procedures should volunteer for testing and,
if infected, should stop doing them.

Groups representing doctors, nurses and dentists last week said infected
health workers pose no danger to patients. They are angry at a draft law
being pushed by Dannemeyer and other members of Congress to force all health
workers to be tested.